The importance of mitochondrial ROS has demonstrated that mice null for Mn-SOD exhibit lethality due to cardiac dysfunction [31], heart/muscle-specific ablation of Mn-SOD produces progressive congestive heart failure [32], and overexpression of a mitochondrial ROS scavenger, peroxiredoxin3, prevents heart failure induced by myocardial infarction [33]. Here, SOD2 is linked to heart failure.