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Since the beginning of this millennium, rheumatologists have become applied cytokine biologists, taking advantage of the plethora of successful “biologics” that target cytokines for the treatment of rheumatoid arthritis (RA) and other autoimmune disorders. The mechanism of action of these agents is to block cytokines outside of the cell. However, the actions of cytokines can also be blocked by disrupting signaling pathways within the cell. This is the mechanism of action employed by a recent class of orally administered drugs, Janus kinase (JAK) inhibitors or Jakinibs. In this issue of A&R, Genovese and colleagues report the results of a Phase IIb study with decernotinib, a second generation, JAK3-selective Jakinib (1).
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Gadina et al. (2015) studied this question.
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