In contrast, mice with cardiomyocyte‐specific loss of Ndufs4 (driven by αMHC) did not show significant structural abnormalities or systolic dysfunction but was found to have aggravated pressure‐overload induced heart failure, and this was associated with increased protein hyperacetylation due to alterations in the redox state and inhibition of Sirt3 activity.9 This evidence concerns the gene SIRT3 and heart failure.