Further, more recently, Veron et al. demonstrated that overexpression of VEGF in podocytes causes nodular glomerulosclerosis, mesangiolysis, microaneurysms, and arteriolar hyalinosis concurrent with massive proteinuria and renal failure in eNOS −/− mice in the absence of diabetes [74], suggesting that increased VEGF activity and eNOS deficiency are sufficient to develop advanced DN-like lesions in mice. The gene discussed is NOS3; the disease is acute kidney injury.