Thus, it is conceivable that in hypertension and other cardiovascular diseases an imbalance between the protective ACE2/Ang-(1–7)/Mas arm, and the deleterious ACE/AngII/AT1 axis of the RAS induces a significant reduction in •NO bioavailability associated with oxidative stress and causes endothelial dysfunction. This evidence concerns the gene MAS1 and Hypertension.