Similarly, genetic variation in endothelial nitric oxide synthase (NOS3) and components of the renin–angiotensin system, including the angiotensin-converting enzyme (ACE) insertion/deletion polymorphism, impair nitric oxide bioavailability, promote oxidative stress, and facilitate endothelial dysfunction—an early and critical event in atherogenesis [30,31,32]. The gene discussed is NOS3; the disease is endothelial dysfunction.