This adverse oxidative stress was implicated to be a potential factor for vascular and renal tubular damage in diabetic nephropathy by increasing the productions of sorbitol, prostanoids, transforming growth factor-β (TGF-β), vascular endothelial growth factor (VEGF), and advanced glycation end-product (AGE) and also by activating common stress-signaling mediators, nuclear factor-κB (NFκB), and protein kinase C (PKC) [4–6]. This evidence concerns the gene VEGFA and diabetic kidney disease.