Indeed, ASH1L, FOXP3 and SMAD3 were significantly downregulated in CD4+ T cells from peripheral blood mononuclear cells (PBMCs) of patients with rheumatoid arthritis as compared to healthy controls (Supplementary Fig. 6; Supplementary Table 1), which indicates that ASH1L and ASH1L-mediated SMAD3/FOXP3 regulation might have potential significance in human autoimmune pathogenesis. The gene discussed is CD4; the disease is rheumatoid arthritis.