Mice deficient in SOD2 die of cardiomyopathy within 10 days of birth, whereas heterozygous SOD2(+/–) mice show ultrastructural damage of the myocardium and mitochondria, associated with an increased oxidative stress as well as an activation of apoptotic signaling pathways in the heart (26, 27). This evidence concerns the gene SOD2 and cardiomyopathy.