In RA, disease-associated single-nucleotide polymorphisms (SNPs) preferentially localize within SE regions in CD4+ T cells, affecting the binding affinity of key TFs and coactivators, thereby dysregulating critical immune regulators such as BACH2, PRDM1, and STAT3 (11, 29) (Figure 4). The gene discussed is BACH2; the disease is rheumatoid arthritis.