Studies have uncovered that overexpressed IRF1 could produce a pattern of hyperacetylation at H4 lysine residues and induce the expression of target genes in vitro, a finding also shown in SLE patients.706–709 Moreover, IRF1 overexpression in monocytes from SLE patients enhanced inflammasome activation.710 Chen et al. reported that HDAC1 inhibited miR-124 and then promoted IRF1 expression to potentiate CD4+ T cell activation in SLE.711 In lupus nephritis (LN) patients, an inverse correlation between IRF1 and miR-130b levels was observed in renal samples. Here, CD4 is linked to systemic lupus erythematosus.