Indeed, treating human CD4+ T cells from healthy controls with the JAK inhibitor tofacitinib selectively targeted rheumatoid arthritis risk genes controlled by SEs (85), while exposure of CD4+ T cells from Juvenile idiopathic arthritis (JIA) patients to the BET protein inhibitor JQ1 preferentially inhibited JIA-specific super-enhancer driven gene expression. Here, CD4 is linked to rheumatoid arthritis.