KMT2A and renal fibrosis: Zou et al. showed that the expression of MLL1-menin and its specific substrate H3K4me1 was increased in a unilateral ureteral obstruction(UUO) model and that MI-503 (an MLL1-menin inhibitor) downregulated the expression of H3K4me1 and inhibited RTC EMT and myofibroblast activation and attenuated renal fibrosis [35].