Several abstracts have studied the mechanism of action of JAK inhibitors (JAKi) in various diseases. JAKi alter many other mediators affected by the JAK STAT pathway. For instance, T cell signature in blood that is proliferative was associated with a response in RA.

Since the millennium, we have seen an expansion in the number of advanced treatments both biologic and targeted synthetic disease modifying anti-rheumatic drugs for rheumatoid arthritis. The challenge remains on how best to characterise the subtypes of RA in order to choose the best drug to ensure optimal outcome for patients. 

Research work from the Accelerating Medicines Partnership (AMP: RA/SLE) Network, was published in Nature and more specifically characterizes RA synovium into several cell-type abundance phenotypes (CTAPs). Could CTAPs known disease features or more effective future therapies?