Intriguingly, induction of inducible nitric oxide synthase (iNOS), not endothelial nitric oxide synthase (eNOS), is required for H2S to block high glucose-induced oxidative stress and matrix protein overproduction in renal proximal tubular epithelial cells, suggesting a role of NO in H2S-mediated beneficial effects against diabetic kidney disease [49]. This evidence concerns the gene NOS3 and diabetic kidney disease.