In AT-II-induced hypertension, NOX-2 activation induces sirtuin-3 (SIRT3) S-glutathionylation which causes acetylation of vascular SOD2 and reduces SOD2 activity, which further results in increased mitochondrial superoxide levels and lessened endothelial nitric oxide bioavailability which acts as an antioxidant in vivo [11,12]. This evidence concerns the gene SOD2 and hypertensive disorder.