The first evidence for the EndMT in renal fibrosis is established by Zeisberg and colleagues, their results demonstrate that a large proportion of myofibroblasts coexpress the endothelium marker CD31 in three mouse models, unilateral ureteral obstruction (UUO), genetic modification, STZ-induced diabetic nephropathy [135], suggesting that these fibroblasts are likely derived from endothelial cells and EndMT may substantially contribute to the development and progression of renal fibrosis. The gene discussed is PECAM1; the disease is renal fibrosis.