KLF1 and ischemia: Previous studies reported that a metabolic shift in neonatal mouse cardiomyocytes from glycolysis to fatty acid metabolism during postnatal development,[36, 37, 38] and inhibition of fatty acid oxidation could promote cardiac regeneration after ischemia in adult mice.[39] Therefore, our results suggest that the metabolic shift induced by the overexpression of KLF1 in cardiomyocytes favors dedifferentiation and regeneration.