Such formation depends on the uptake of circulating AGT.31,35,73 Indeed, in DOCA-salt hypertension, AGT siRNA did not affect blood pressure, yet did reduce the heart weight/tibia length ratio, a marker of cardiac hypertrophy.18 Since this effect was accompanied by the disappearance of cardiac Ang II, this likely represents the fact that AGT siRNA is capable of blocking Ang II formation at cardiac tissue sites. The gene discussed is AGT; the disease is cardiac hypertrophy.