The Ang-II contribution to the pathophysiology of cardiac and kidney failure is mainly based on the following observations: (1) Ang-II is produced within the myocardium and renal cortex, (2) Ang-II is activated within the failing hypertrophic heart and overproduced in hypertrophic kidneys, and (3) the pharmacological inhibition of the RAS and Ang-II in either animal models or in patients with a hypertrophic heart and injured kidney showed high effectiveness. The gene discussed is AGT; the disease is benign neoplasm.