Angiotensin II (Ang II), the major mediator of RAAS,[3] increases water reabsorption in the kidneys and induces vasoconstriction, thus increasing blood pressure.[4] Sustained RAAS activation will lead to the development of HTN[5] which will cause endothelial dysfunction by creating an imbalance between relaxant (mainly nitric oxide) and contractile (mainly Ang II) endothelial factors. The gene discussed is AGT; the disease is hypertensive disorder.