In addition, cardiac-specific ablation, or pharmacological inhibition of pyruvate dehydrogenase kinase 4 (PDK4), which physiologically inhibits mitochondrial pyruvate dehydrogenase thus improving cardiac fatty acid oxidation, induces cardiomyocyte proliferation and improves cardiac function after myocardial infarction (64). This evidence concerns the gene PDK4 and myocardial infarction.