Third, in vitro data suggest that IL-6-induced STAT1 phosphorylation is more strongly inhibited by tofacitinib than IL-6-induced STAT3 phosphorylation in T cells (17, 18), whereas we demonstrate comparable inhibition of both IL-6-induced STAT pathways in CD4+ T cells of RA patients in vivo. The gene discussed is SOAT1; the disease is rheumatoid arthritis.