The production of IL-17 and IFN-γ from CD4 T cells in peripheral blood may directly contribute to the pathogenesis of RA (Park et al., 2014), while TNFSF10 may selectively activate CD4 T cells to promote IFN-γ production (Tsai et al., 2004), indicating that TNFSF10 may be a potential therapeutic target for RA. This evidence concerns the gene CD4 and rheumatoid arthritis.