EndMT has been implicated in renal fibrosis in diabetic nephropathy, with up to 30–50% of FSP1/α‐SMA‐positive cells co‐expressing the endothelial cell marker CD31 in diabetic mouse models.[50] Consistent with this, the results of this study showed decreased expression of the endothelial marker VE‐cadherin and increased expression of fibroblast markers vimentin and α‐SMA in high glucose‐stimulated HUVECs, indicating EndMT. This evidence concerns the gene PECAM1 and diabetic kidney disease.