VEGF‐induced angiogenesis contributes to the pathogenesis of DN34, 35 and antibodies directed against VEGF have been shown to prevent proteinuria and glomerular hypertrophy in animal models of diabetes.36, 37 Previous studies demonstrated that activation of PTPN2 contributes to the suppression of VEGF‐induced endothelial cell proliferation and angiogenic sprouting.38 Consistent with these results, we found that angiogenesis using CD31 as marker was significantly increased in kidney in the diabetic group. This evidence concerns the gene VEGFA and diabetes mellitus.