Oxidative stress and vascular NO bioavailability imbalance represent the major etiopathogenetic factors of vascular injury and hypertension [41], with angiotensin II and RAAS acting as crucial triggers of ROS production (e.g., by angiotensin II-induced activity of mitochondrial NADPH oxidase 4, NOX4, which is the upstream signaling molecule of ERK) and endothelial NOS (eNOS) inhibition [42,43,44]. This evidence concerns the gene AGT and Hypertension.