COX-2 is the principal source of intravascular reactive oxygen species creation, and, in arterial hypertension and diabetes, this seems to be the result of an interaction between COX-2-induced prostaglandins, lower activity of oxidase, RAAS, nicotinamide adenine dinucleotide phosphate, and bone morphogenic protein 4, as a concentrated pathophysiological cascade in stimulating and preserving endothelial dysfunction [155,156]. The gene discussed is PTGS2; the disease is Hypertension.