Importantly, our results suggested that blocking type I IFN signaling with Tofacitinib strongly repressed the VGLL3-induced ISGs expressions, indicating that VGLL3 might drive the IFN-β1 expression by activating IRF3 and secreted IFN-β1 stimulated the ISGs expression in RA-FLS in an autocrine manner. The gene discussed is IRF3; the disease is rheumatoid arthritis.