Overexpression of Bnip3 in the heart shortly after birth triggers dilated cardiomyopathy starting at 10 weeks of age.26 This stands in contrast with the cardiac atrophy phenotype induced by caFoxO3 activated in young adult mice, even though Bnip3 levels were increased dramatically, as well as our observation that Bnip3‐null mice were resistant to the atrophy‐inducing effect of caFoxO3. This evidence concerns the gene BNIP3 and dilated cardiomyopathy.