EZH2 and Hyperglycemia: Previously we observed that glycated-BSA, diabetes, and hypoxia reduced EZH2 expression in differentiated podocytes and renal glomeruli [18,64], while in human aortic endothelial cells hyperglycemia induced EZH2 expression and increase the repressive mark H3K27me3, thus contributing to endothelial-to-mesenchymal transition (endoMT) [65,66].