Several lines of evidence implicate ROS in the development and progression of heart failure (reviewed in [25]): first, the levels of ROS are elevated in both plasma and myocardial tissue in heart failure; second, hypertrophy and apoptosis of cardiac cells in response to neurohormones such as norepinephrine, ANG-II, or cytokines appear to be modulated by redox-sensitive pathways, as the administration of scavengers of ROS diminishes cardiac remodeling after myocardial infarction, a condition characterized by increased generation of ROS. The gene discussed is AGT; the disease is heart failure.