As the aging process, per se, is associated with higher ROS formation rates, especially from mitochondria, these “oxidative stress aging conditions” can be mimicked by a deficiency in antioxidant enzymes, e.g., manganese superoxide dismutase, leading to more pronounced eNOS uncoupling, endothelial dysfunction, and higher blood pressure in Ang II-treated manganese superoxide dismutase deficient mice [9]. The gene discussed is SOD2; the disease is endothelial dysfunction.