Hypercholesterolemia in FH patients induces the generation of superoxide radicals that may reduce the activity of endothelial nitric oxide synthase (eNOS) and react with NO; these events result in the reduction of NO bioavailability as an antioxidant and vasodilatory compound with the consequent inflammatory response in the vessel wall [17]. Here, NOS3 is linked to familial hypercholesterolemia.