Given that type I IFN signaling utilizes JAK1 and tyrosine kinase 2 (TYK2) as signal transducers, JAK inhibitors—some of which are already approved for rheumatoid arthritis (120) —show potential by blocking IFN-α and IFN-γ signaling, particularly in monocytes, as well as in other immune cells (121). This evidence concerns the gene TYK2 and rheumatoid arthritis.