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]. The gene discussed is SIRT3; the disease is Hypertension.