Earlier this year, Dong and colleagues demonstrated that the application of rapamycin, in high glucose-induced human renal glomerular endothelial cells could significantly increase platelet and endothelial cell adhesion molecule-1 (CD31) and vascular endothelial-cadherin expression, while reversing the over-expression of Collagen 1 and α-smooth muscle actin and alleviating endothelial-to-mesenchymal transition (EndMT), which plays a key role in the development of DKD [34]. This evidence concerns the gene PECAM1 and diabetic kidney disease.