The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway in FLS is indirectly activated by the tumor necrosis factor (TNF) through the autocrine expression of type I interferon (IFN), resulting in IFN-α/β receptor engagement and the production of chemokines by T cells, which play a role in the effects of the JAK inhibitor CP-690550 (tofacitinib) in the treatment of RA. This evidence concerns the gene TNF and rheumatoid arthritis.