In DKD, endothelial GR knockout diabetic mice displayed higher relative area of fibrosis and collagen deposition, significantly upregulated α‐SMA, increased active β‐catenin levels and significant CD31 downregulation in renal ECs compared with diabetic control mice, suggesting that GR deficiency mediates EndMT in ECs in diabetic kidney disease by upregulating Wnt signalling, ultimately promoting the progression of renal fibrosis and glomerulosclerosis.72 This evidence concerns the gene PECAM1 and diabetic kidney disease.