One of the potential cardioprotective mechanisms of SIRT3 is to regulate the deacetylation of enzymes involved in mitochondrial metabolism, including long-chain acyl CoA dehydrogenase (LCAD) and β-hydroxyacyl CoA dehydrogenase (β-HAD) in fatty acid β-oxidation, pyruvate dehydrogenase (PDH) in glucose oxidation, and enzymes of the tricarboxylic acid cycle and the electron transport chain, while hyperacetylation of the aforementioned enzymes can impair cardiac energy production in heart failure [162, 167–175]. The gene discussed is SIRT3; the disease is heart failure.