Endothelial dysfunction and most cardiovascular disease are characterized by increased levels of ROS formation due to an imbalance between pro-oxidative enzymes (xanthine oxidase, NADPH oxidase, uncoupled eNOS or enzymes of mitochondrial respiration) and antioxidant enzymes (Cu, Zn-SOD, Mn-SOD and extracellular SOD), resulting in a deviation of cellular redox environment from the normal [64]. This evidence concerns the gene NOS3 and endothelial dysfunction.