Xu et al. (54) found that when hemodynamic loading conditions remain unchanged, cardiac Ang II does not elicit hypertrophy but in animals with hypertension, cardiac Ang II, acting via AT(1)R, increases oxidative stress, inflammation, ventricular hypertrophy, and cell death (probably via down regulation of PI 3 kinase and Akt). The gene discussed is AGTR1; the disease is hypertensive disorder.