Recently, Nox4 was shown to be implicated in kidney diseases, such as diabetic nephropathy, and damage to the kidney induced by other pathways of renal damage, including advanced glycation end-products, the renin-angiotensin system, TGF-β, and protein kinase C. The role of Nox4 as a target for renoprotection remains controversial, although recent positive preclinical data have stimulated increased interest in inhibiting the enzyme in clinical trials of renal disease [2]. This evidence concerns the gene TGFB1 and kidney disorder.