Actually, regarding our previous finding that constitutive STAT3 phosphorylation is common in circulating CD4+ T cells in RA and associates with disease activity (8), one mechanism implementing the efficacy of tofacitinib in treating RA might be the relatively good inhibitory effect on CD4+ T cell STAT3 phosphorylation in vivo. The gene discussed is STAT3; the disease is rheumatoid arthritis.