The assertion that Ang II is essential for the pathogenesis of cardiac hypertrophy is further buttressed by the observations that either blockade of its synthesis (by the angiotensin II converting enzyme inhibitors) or disruption of its signaling cascade (by genetic deletion of its receptor/AT2R or by administration of AT2R antagonists) is cardioprotective in rodents and in patients with heart failure (Opie and Sack, 2001). The gene discussed is AGT; the disease is heart failure.