In accordance with these findings, KMT6A inhibited mesangial cell proliferation and fibrosis-related protein expression in hyperglycemia-treated mesangial cells by downregulating hairy and enhancer of split 1 (HES1) expression; a ChiP assay showed that the KMT6A and H3K27me3 levels were increased in the HES1 promoter and enrichment was intensified by KMT6A overexpression [97]. The gene discussed is EZH2; the disease is Hyperglycemia.