Interleukin-10, IFN-α, and IFN-γ are also likely contributors to RA pathogenesis, and inhibition of these responses may contribute to the mechanism of JAKis in RA treatment; lesser inhibition of IL-10 may be desirable as the net effects of this cytokine have been described as anti-inflammatory in RA [4, 24]. Here, IFNG is linked to rheumatoid arthritis.