Day 4 Recap: EULAR 2026 Save

Hello everyone. Welcome to RheumNow's daily recap from EULAR 2026. It's day four, the final day. We're delighted to have been here, but even more delighted to go home. I'm going to introduce today's panel. I'll start with myself. I'm Dr. Jack Cush from Dallas, Texas. Dr. Day, I'm Ralini Day. I'm a rheumatology fellow in London in the UK. Dr. Ysef. Hello. My name is Dr. Ysef and I'm from Leeds and I'm actually home. The benefits of being in London. And Dr. Chan, I'm Anthony Chan. I'm from Reading, United Kingdom. Are you home? I am about to leave now. I'm still here. Okay. All right.

So, what we do in these daily recaps is I have our faculty who've been scouring the meeting and doing a fabulous job of covering this in social media and writing and video and podcast. I asked them to come one evening after the day and just tell me what they thought was great. Even though they all have different assignments and topics that they're married to, they can freewheel and do whatever they like. So, let's start with our first round with Dr. Day.

Yeah. So, I'd like to cover one of the late breakers that were presented today. This was LB 00005, baricitinib in early PMR. Where we've got very limited treatments, although you know we did hear about the updated guidelines today as well. So this was a double-blinded randomized parallel group phase three study with 46 patients with early PMR randomized to baricitinib 4 milligrams daily or placebo alongside a rapid steroid taper from 20 milligrams to zero over 11 weeks. And essentially at week 16, glucocorticoid-free remission was achieved in 65% of the patients receiving baricitinib as opposed to just 17% who were on placebo, and baricitinib also reduced the relapse risk and lowered the cumulative steroid exposure. In terms of safety signals, they had one serious adverse event in each of the treatment arms. So essentially baricitinib significantly improved the chances of achieving steroid-free remission in PMR and suggests that JAK inhibition could emerge as an important steroid-sparing agent. We do of course probably need larger studies though — that's the key thing.

So yeah, let me ask the other panelists what do you think about — is there going to be a future role for JAKs in PMR? Anthony, what do you think?

Yeah, I think it's great. The results were quite good. 65% could be glucocorticoid-free versus 17% on the placebo — that's quite significant. There's a lot of morbidity from long-term prednisolone use in these patients and often they find it quite hard to taper as they come towards lower doses. So I think if we can get them off quickly, I think that's going to be a positive thing. We have to just be careful about the long-term effects, and these are probably older patients who are going to be using this therapy for PMR and how that weighs on their thrombotic and cardiovascular risk.

Yeah. So I think there's a role for JAK inhibition, as we also see with baricitinib. The question will probably be asked by everyone: after you achieve this remission, what happened? Because in part three of this study they did show that once baricitinib was discontinued after 6 months, there is a numerically increased frequency of relapses in those who discontinued compared to those who continued. So we do need longer follow-up and also larger numbers, like what Dr. Day was saying just now.

Yeah, what that brings up is that it was numerically higher but the numbers at that stage of the study were small so you can't really talk about significance, but it does say that PMR patients need therapy for more than a year. And another critique I've heard is that this was an 11-week steroid taper — and you know, who in their right mind aims for an 11-week steroid taper? Well, the makers of this study, because JAK inhibitors have a fast onset and maybe JAKs can take up the slack when you get them off steroids, and maybe it's a safer kind of thing.

So I just want to bring up something — I know that you want to talk about this, Dr. Day — and that is, right before this there were the new PMR/GCA guidelines, and in that guideline, number three out of 12 recommendations was that in new-onset PMR, oral corticosteroids should start at 12 to 25 milligrams and be tapered to 10 milligrams within two months — 8 weeks — with the goal being to stop steroids within a year. So the goal of this particular study was particularly aggressive, but again they were using aggressive therapy. So how do you think the study fits in with the new EULAR guidelines?

Um, so firstly I'm conflicted because I am a fellow on that guideline. However, I think one of the things we've seen is that there are limited agents for steroid-sparing
agents in this disease and that was shown beautifully actually in the guideline because we have suggested using IL-6 inhibitors and then methotrexate has actually stayed in the guideline despite the fact that we've got limited evidence as our SLR which is due to come out will show. And so actually having these results is encouraging in the sense that perhaps there are more drugs on the way that we could use, just as we've seen in GCA. But yeah, I think we need to treat it cautiously for now because as we've discussed the numbers are low, the time is also low in which this was tested.

So yeah, for those of you a little confused at home, SLR is not a camera. It's a systematic literature review, which is a gigantic part of any guidelines effort, and Dr. Day was one of the people who has to put in hundreds of hours to get the literature that informs the guidelines. But yeah, I thought that was a very interesting study.

So what's your big one for today? Yes, I just want to present abstract LB00003 that was presented at the late-breaking abstracts. So this is not to change our practice now but certainly something to watch out for tomorrow or in the future. So as we know there is some limitation of CAR T cells, you know, with the conditioning, the time process, the problem with manufacturing and also accessibility and scalability. So therefore we need others in the therapy that can address this. So one other way is to do an off-the-shelf therapy.

So this abstract is about the development of an off-the-shelf NK therapy. The compound is AB101. So this was a basket study. The study overall is actually looking at four conditions: severe refractory rheumatoid arthritis, we have Sjögren's disease, we have severe refractory systemic sclerosis, and also idiopathic inflammatory myopathy. But the authors presented only for three diseases, excluding myopathy — I'm sure we will see that in the next conference.

So in this study they showed a preliminary analysis. In order to administer this compound, this can actually be administered as an outpatient in their day case unit. However, it does need a few things. Basically they need to receive low-dose cyclophosphamide and fludarabine, and then after that they will then need the treatment itself which is given 7 days apart. And then after that they also need a course of rituximab. So basically you've got this three-combination therapy, and these are really needed because these patients are refractory — for example, like rheumatoid arthritis, they have to fail more than two biologics.

So the preliminary results do look encouraging up to 52 weeks. For example, in rheumatoid arthritis the endpoint was ACR50, so it's quite a higher-hurdle endpoint, and they did show about 71% reduction at 6 months. This is — we can't do a direct comparison — but the REFLEX trial in rheumatoid arthritis years ago, back then Professor Emery, so that was a failure of one TNF inhibition and the ACR50 was around 30%. So if you just look at that, you know, it is quite impressive from that point of view. And certainly they did look at some good signals as well in terms of Sjögren's, in terms of changes in ESSDAI, and also patient-reported outcome improvement as well. And also in the systemic sclerosis there's not much significant safety signal in the short term — they don't see any more than grade two CRS or any ICANs at all. But certainly this is preliminary. The results are up to 52 weeks, so we don't know what happened longer term, whether the patient may relapse and whether they need redosing, whether redosing is effective, because sometimes with all this allogeneic therapy you might be concerned about graft-versus-host rejection and so forth. But certainly something that we need to look into, and also they will need a comparator group — having a single arm is quite difficult to interpret.

So I can go a lot of ways here, but let me ask the other two panelists. Where are we in your head regarding CAR T? And I don't want you to say what you just said, or I don't even need you to endorse CAR T. We've had now three years of CAR T anecdotalism, and are you ready for this? And what do you want to see and where is this going to go? Anthony, why don't you tackle that? Give me 30 seconds on that.

The issue is we don't have a lot of controlled studies in these CAR T studies. So if you had further B cell suppression for example in another arm, whether we would see a difference with the cellular therapy, and then there is the allogeneic versus the autologous forms as well, whether there are any differences. So I think at the moment we will probably use this in
our most refractory patients and Dr. Day. Yeah. No, I think we're still in very early stages even though it feels like we've been talking about this for a long time now. Um, but we are still in very early stages and as Y was saying the longer-term effects we don't quite know. Um, as well um and certainly from like just from what I see in in clinic it is very much the the very refractory ones that we are putting forward for for trials and things. So yeah.

So use other than learning a new tool and the many sides of this new tool in different ways. This is an off-the-shelf uh version which is certainly unique uh and learning about safety. What else has come of the CAR T-cell therapy thus far?

Yeah. So I think uh apart from I think that there's there there's a way in terms of trying to improve the the targets as well. We you know we have seen you know the abstract presented 3 days ago in the first day of EULAR um you know so we thought that you know ki will be eternity you know patient had this really intensive in the beginning they were that's long certainly looking at the lupus cohort was quite impressive I think there's one track saying like the no relapse up to four years but you know altogether you know with 50 patients that have been treated with the original Erlangen cohort you know of you know of CD19 CAR T there actually about 12% people had relapse and this was severe relapse and then sometime that that just made think whether this patient whether is CD19 the right target whether you should you have targeted CD you know BCMA for example to reduce you know to remove the you know plasma cells in the beginning but then also you have to find the balance between in term of long-term with low you know IgG which can increase risk of infection vaccination response and so forth so there's a lot of questions to ask but also we also have to find the balance participation so so refractory so they failed a lot of things so I think cost effectiveness um analysis really important here I think people not really talking about it I think it's really key.

Yeah yes and and and we can't get into this because we can go forever but um Dr. Yousef and I had a you know a poster side conversation about this and you know a lot of people doing the planning haven't you know planned for the fact that you're going to make people hypogamma um and you know worry some sort of low IgG levels so that now they need to be treated with gammaglobulin and that you know is so there's now an infectious risk uh that has an expensive solution to so again I I think I like that you know learning the dynamics of response and and then reconstitution, you know, and learning how to do. I think these are all valuable lessons, but I think we're all anxious to start seeing controlled real trials going forward.

Um, Anthony, what's your your your favorite for today? Uh, my favorite today was the Big Bowl uh late breaking 001, which is the um study between bimekizumab, the IL-17AF head-to-head versus risankizumab, the IL-23 inhibitor. Uh the data at 16 weeks uh and showed a 50% ACR50 versus around 38% in the risankizumab and also at four weeks there was a three-fold improvement in the bimekizumab group versus the risankizumab group. So I think we now have a head-to-head in um in the joints for PsA. We've had skin data before but this is quite useful um in terms of understanding the mechanism of action.

Yeah, and I think you know there was a it was a great presentation by Morola. You know, first it started as a press release, then an extended press release with some data. Now we saw not just week 16 data, which was good, but week 24 data. Um, and the ACR50 looks great. Are you bothered by the fact that the secondary endpoints weren't significant? You know, MDA skin, you know, whatever. They they they weren't significantly different. um um and there was might have been an edge but it was not significant. This is pretty well-powered trial. So that's one thing that makes me concerned. The other thing is why did this head-to-head trial work when so many other head-to-head trials have failed? Um in the in PsA, you know, so many head-to-head trials are clearly winners in PSO, but in PsA, head-to-head, why did this one work? So you have an answer for either of those things?

I think the IL-23 uh I think still has probably a bit more superiority in in skin compared to joints. So but this came the other way around with the more these people had quite low skin scores. They didn't have very high skin scores in this study. Hence they didn't probably the MDA has a skin component to it and probably that's why it couldn't meet all of the seven components to achieve MDA. Yeah.

Um, and I think you're you're right, but there are actually now head-to-head um um bimekizumab against 23s and the dual inhibitor has has outdone the 23. So it's a little bit of an argument in the derm world which is the better drug um when it comes to you know best PASI 100 response but it clearly you know 23 really does
very well and as does the dual inhibitors compared to the single uh IL-17A inhibitors without the F. So it's a really interesting study. I think it will cause a fight.

If I asked you — and the three of you in the UK — you wouldn't know the answer and I didn't know the answer, but supposedly the best-selling biologic right now in psoriatic arthritis in the United States is actually risankizumab. Now collectively all the IL-17s are going to outdo — you know, the IL-23s would be my guess — the other one being guselkumab as an IL-23 inhibitor, but it's a very competitive market there. Companies are spending a lot of money and doctors are really confused because they've got more PsA drugs than they have PsA patients. And that creates a lot of choice indifference — or choice overload.

All right. So my number one is, I think, almost a monumental study. It is the follow-up to ORAL Surveillance. And you're thinking, ORAL Surveillance? There's another one of those? Are you kidding me? Well, no, there wasn't. But there was a follow-up that was FDA-mandated for baricitinib to look at the VTE risk in patients taking a TNF inhibitor versus baricitinib 2 or 4 milligrams a day. So it was a post-regulatory commitment, and patients were enrolled — over 3,500 patients, I think — who were at risk for VTE by either having had a prior VTE, being over age 60, or being obese. And so they had, like ORAL Surveillance, they were trying to stack the odds for the events, but it wasn't quite the same — but then again maybe it was pretty close.

And in the end, you know, they had 3,600 patients enrolled. They followed them on average more than four years. And there were two studies: there was the RA-BRIDGE and the RA-BRANCH study. One was a global study, one was a US — similar but smaller — study. They combined them, and in the end clearly baricitinib, both doses, individually and combined, gave you significantly more venous thromboembolic events. So this mirrors the results of — first, tofacitinib when it was first approved by the FDA and other worldwide regulators — that VTE risk was there from the start. If you remember, tofacitinib had no VTE risk in its label when it started out. It was only after ORAL Surveillance that they all got slapped with it.

So anyway, this data now reinforces the original baricitinib label and the extension of the ORAL Surveillance risk for VTE to all JAKs and probably TYK2 inhibitors. But unlike ORAL Surveillance, the two doses — either dose of baricitinib — did not increase major adverse cardiovascular events, MACE events, nor the risk of cancer, nor the risk of opportunistic infection, nor the risk of arterial thrombotic events. It did show a significant increase in serious infectious events, somewhat like ORAL Surveillance.

So the question is, what does this do? Does this create confidence or does it make you still worry? I'm going to ask each of you to answer that. I'll let you think about it for 10 seconds, but that's kind of where this goes. Is this data that doesn't change your prescribing — what you already know from ORAL Surveillance — or does it make you more worried or less worried? Who wants to go first? Minnie, why don't you go first?

Yeah, I think a couple of things. Firstly, I think it's really encouraging, the results about the MACE and the malignancy, just because this was actually a population-enriched cohort who supposedly had greater risk factors for both of those things. But I think yeah, it needs — as we discussed in a separate video earlier today — it needs to be treated with caution, probably the results of course as well. The targets of the two drugs are different: baricitinib and tofacitinib. This is only two JAKs, whereas that's three. So yeah, I'm not sure it would change my practice just yet.

Okay, Anthony?

I think change — or caution — that's people who are above the age of 60, BMI greater than 30, previous VTE: consider whether there are alternatives before we go and use the JAK.

Let me just give a little perspective on what you just said. I agree with you 100%, but it's a little bit like trying to achieve an ACR20 — which is not a low-level response; getting a 20% response out of seven variables, at least five out of seven — it becomes successively harder. Hence recruiting patients who go on JAKs when you restrict it to over age 60, BMI over 30, having failed one prior — the idea is, you know, the people who are at highest risk in ORAL Surveillance — over 65, smokers with a cardiovascular event — that's like 8% of my JAK PsA audience. I think the same thing applies here. And I do think caution is necessary, but I also think being real — understanding that you can't apply this caution to everyone, because now you've cut off a valuable treatment arm in your arsenal.

Up or down?

Yeah. So I'm cautiously optimistic. I
think that's what it is. Yeah. Um I mean the the risk for VTE is in line with with with the label um in the safety profile that we know from before. Uh but um you know the it's a bit difficult in terms of the the the selection I know you said like maybe quite quite the same pool but it is a bit different because like this one is like you have to have one VTE risk factor whereas in the ORAL Surveillance you have to have one um you know risk factor for MACE um yeah so maybe in but not not all so I mean do we need another ORAL Surveillance but in baricitinib and or another ORAL Surveillance in for example so I think it's all got up in the there there but I think you know that that data give you slightly more more more reassurance you know you know than than what it was before. Yeah.

All right. So again I I I will just say that I think this firmly establishes VTE and SIE risks with JAK inhibitors over TNF inhibitors. I think it murkies the conversation considerably about cardiovascular and cancer risk. Um because these are two very large randomized controlled trials. Now with you're looking at over 8,000 patients all followed for more than four years. That's more than 32,000 patient years. I don't care what report you're going to see from some cohort, you know, from Portugal or some reconstructed, you know, claims data that's trying it. None of it matches these two studies. These two studies give you the best data from which you have to make a decision to be cautious, overly cautious, minimally cautious. It's up to you.

All right, we're going to do one more. We're going to do quick hits here. 30 second descriptions, a few comments and let's let's uh move on. Let's start with Dr. Yusuf. Yeah. So just um John trying to um discuss about abstract LB00007. Um so this is an extension or extrapolation of uh promising therapy using uh FcRn receptor blockade. Uh the compound is nipocalimab. Uh as we all know so the last uh couple of years we have had uh uh results presented for nipocalimab and also efgartigimod which is another FcRn receptor in Sjögren's disease which they've now finished recruitment in phase three so we probably be listening to results in the next 18 months but this one is for SLE um so basically this is a patient with a moderately uh moderate to severe active SLE so they did have uh over 200 patients that were randomized so into three groups. One is placebo, one is nipocalimab with 5 milligram per kilogram IV infusion one and another one is 15 milligram per kilogram.

Um so the results uh show that the primary endpoint which was the uh SRI-4 um was met uh in the higher dose group. Um so basically the effect size was about 14%. Um so 53 54% um for the nipocalimab and also um 40% um in the placebo again there's an issue with placebo response here you know with the lupus trial so usually up till you know 30 to 50% it may be because they're not really they did try to mandate the steroid taper from week 6 to 16 and after you know uh you know you have to be less than 7.5 milligram per day but after that is dependent on the discretion you know for that as as long as it didn't go up. Um I think because of that it's still a bit lenient. So if you compare to other trials more successful for example um like the anifrolumaб phase 2 they did ask to go all the way down to 5 milligram per day then they see a lot of major difference and reduce placebo response and that may be the case.

So in this case like you know it did show like you know the primary endpoint was you know was demonstrated and also they did do some subgroup analysis where they did say like you know if you stratify them in patient with high interferon you know very active antibodies you will get better response so I'm just want to highlight one thing potentially so in terms of like safety um so they did say about 23% people had low IgG uh although they did say that you know this patient didn't have any uh you know serious infection but certainly this is something you know to look out for in in the longer run and I think there were two patients also um you know had pneumonia and things but you know certainly it will go to phase three and one thing that I quite like just quickly one is I like the name I mean I like the name yeah so the name is like you know this one is called JASMINE and the phase three which is currently undergoing is called GARDENIA there you go yeah well again there's a lot of buzz around FcRn receptor drugs and they do a really good job of lowering autoantibodies, but that isn't necessarily an end point. It shouldn't be an end point in antibody-driven disease like lupus. It might pan out. So, this is encouraging, but I I don't know that it's going to I I again, there's a number of these that are in development in a number of disorders, and I'm very cautious about interpreting, but I like this result. Let's go on to the next one. Dr. Day, what's your last one? Um, so I'm actually not going to talk about
an abstract, but I'd like to draw attention to the plenary sessions which are available to rewatch and particularly the uh rheumatoid arthritis one today, which was um a really good overview. It was by Dr. Nikki Faru. Uh a good overview right from the beginning of where we started in terms of treating RA several years ago right up until the current day with the trials that we've had on um potentially preventing the onset of RA um and really highlighting the landmark um papers that have happened in between on difficult to treat RA and the comorbidities in RA um and uh it was really a good reminder of uh well essentially of how far we've come but also I can recommend sending it to people who weren't able to come to EULAR. Uh a really good overview of uh all things rheumatoid arthritis.

Is there proof that all these great advances actually has done anything really important uh like um you know ACR 20/50/70 who cares? They all look the same uh in in the end. And I know we're very good at managing RA and we're very good at patting each other on the back but RA is still a deadly disease. So what's the proof — what proof did she say that these really have changed the outcomes?

Well actually she was talking about how perhaps we are in our drive to develop new drugs we are forgetting the other aspects around the drugs which which matter. So uh you know we we are better at managing comorbidities but we you know we still got a long way to go. Then there's also the kind of the bits that I'm interested in like the health equity, the social determinants, that side of things as well, which we're maybe not quite so good at — looking at things like fatigue, pain syndromes, um you know, what do we actually — mental health? Yeah. Mental health. So all of that as well.

Um, and I, you know, I was having a conversation earlier in the congress with somebody saying that perhaps we've forgotten a little bit about RA in our in our drive to like try and improve the treatments in other in other areas as well. So, I think there's more work to be done in RA. Actually, I don't think we've quite reached our, you know, the peak as yet.

Well, again, I think the evidence is also that mortality rates are down um and have trended down since the biologic era and surgeries are way down, uh hospitalizations haven't really changed all that much. Um but you know, the question is is that because of biologics and advanced therapies, I think we um we assume that and I think it's — I assume that, but I can't prove that. But what I — here's my worry. My worry is we all think we're pretty darn good at RA, which means that there's no urgency on RA and I think you just need to have one or two of your RA patients die prematurely to be reminded that we're not as good as we think we are.

Dr. Chan, what's your last one? Uh, my last one is the sonelokimab, the nanobody, the IL-17AF. We've heard about it in PsA today. We heard about it in axSpA — both radiographic and non-radiographic. This is a phase 2B. It's a single arm study so there were no controls but it showed positive response in ASAS 40 and also they had PET scan results. They had a fluoride um uh PET scan which measured uh the uptake and they had reduction in the overall uptake and also in the sacroiliac joints in this study. So more from a mechanistic point of view rather than a sort of true efficacy because we don't have a control in this study. But I thought it was interesting that uh the size um of this molecule maybe has a role to play uh in terms of its um long-term uh benefit.

So that's like the thing that companies will do, right? You know, they'll they'll take a drug that looks like another drug. You know, this is a dual IL-17AF inhibitor like another one that was just talked about in the BOLD study that looks really good, but this one's new because why? It's a nanobody and they got to market the heck out of that telling you that that means something. What exactly does that mean other than the size, you know, show me the money? Um, you know, as Cuba Gooding Jr. said — which is I don't care about your PK, your human versus chimeric versus — I don't care what versus, you know 12 microns versus 400 microns — show me that it works. You know, and one of the things that I like that I heard from you know all the people that you run with Anthony in the uh spondyloarthritis world was that the supposition that maybe this would be better at penetrating enthesitis and these drugs — these diseases being really enthesopathies at their origin — which would either result in less enthesitis or maybe better outcomes, better — but again these — that's all talk. Well what I mean — do you have any different perspective now because this is a phase three trial — this is — there there's been a few trials of this. I think it's good, I think it's going to get to the market, I think we're going to hear these discussions when we talk to our colleagues or to the companies. Yeah, I think we — well, I'll have to see when
it gets to phase three and whenever a, you know, comparator another head-to-head that would be interesting. So, my last one is um born of, you know, walking the poster floor and um and it's hard for me to do because so many nice people want to do selfies and talk about RheumNow and and that's all great, but I got to I got to learn something. And then even worse, I see my friends, you know, and I'm walking by and there's Atul Deodar standing talking to some gal about something and and he starts, you know, waving at me and waving me over and I, you know, I'm going to go over because he's a great guy. He's a great teacher. I learn from him all the time. And I don't really want to look at his poster because it's about, you know, it's a drug company study and I don't really I don't, you know, anyway, it was an interesting study.

It's actually a poster on the SELECT-AXIS 2 study which was a phase three randomized control trial of 734 patients with radiographic or non-radiographic axSpA who were treated with upadacitinib 15 or placebo and it worked really well. But of the 734 patients at the end of the trial at week 104, 194 were in remission and then they were randomized um I think to either continue or or to stop. Uh and no actually I think they all stopped and then and they followed them and the interesting thing was um that 78% of them flared. So obviously you don't want to stop you know a powerful JAK inhibitor like upadacitinib that was working um because 78% are going to flare but the other there's two really interesting caveats to here.

One that when you retreated them you know almost 90% of them regained their low disease activity status um uh within six months. So that's encouraging that you could stop and always go back to the the thing that worked before. But then there's this crazy story of 22% went off the drug and maintained drug-free remission for more than 48 weeks. Who are these people? They were bad enough to get into axSpA with active axial spondyloarthritis. They benefited from it and then you stopped it.

So I told the story and there there was two people there along with uh uh uh Dr. Deodar, you know, put three or four rheumatologists together, you'll get seven opinions. And they all agreed with me. The story is it's a young male with ankylosing spondylitis in the non-steroidal era. He didn't want to go on a TNF inhibitor. He kept saying, "Dude, dude, try it. It's a silver bullet. You'll feel fabulous." And finally they do it and they come back and say, "Why didn't you make me do this? I feel so good and I'm doing great." And then the interesting thing happens is that that after a year or two or three, they stop the drug that was working, but then they stay in remission and they don't want to go back on whatever drug it was you put them on.

So, does this mean that there's something about spondylitis that it needs a big hammer to, you know, to knock it down and maybe that can have long-term benefits in one out of five patients?

Anthony, what do you think? There are some patients who stay on NSAIDs for long periods of time and the disease seems to be very well controlled. There's no structural change. So probably this group of patients who are now on top of that are also probably getting um you know JAK inhibitors when their scores went up. It could be that group who in the past would have maybe maintained them on long-term NSAIDs because there was another um the FAST-LANE study also presented here which also showed that if you went with NSAIDs plus JAK you do better uh than the NSAID alone. We are probably looking at this group of people who would have responded quite well to any any anti-inflammatory type treatment hard at the start.

All right. Any any other comments on on this one? Okay. If not, let's go. Go ahead. Wasn't any um the difference in term of disease duration whether was it like shorter disease duration or these patients? Do you know? Uh I don't know that that that that was not available in the poster. I think that's a certainly a reasonable um thought that maybe shorter duration disease might have been self-limiting in some way as opposed to someone who's had disease for you know 10 12 years which is often the case in patients enrolling in axial spondylitis trials they usually have long disease durations but um that's an interesting thought um but don't be I guess the point is don't be surprised when this happens and and I'm glad that um I got stopped by um a major character like Atul Deodar.

All right, everyone. Thanks so much for all your hard work this week at EULAR. Um get some rest. Uh enjoy each other's coverage and um next week we're going to once we're all back home and rested, we're going to do a few panels uh topic discussions and um the audience can watch those. Uh I think it starts next Tuesday um at the same time as as this this program. All right, folks. Thank you so much. Bye-bye.