In order to gain some insight into what extent these leukocyte signaling aberrations are normalized by tofacitinib treatment, we compared the differences in constitutive STAT phosphorylation between controls and RA patients (historical data) to those between tofacitinib-treated and untreated RA patients derived from the current study (Supplementary Table 5). The gene discussed is SOAT1; the disease is rheumatoid arthritis.