A recent study showed that the SGLT2 inhibitor empagliflozin can improve heart failure and adverse cardiac remodeling by enhancing the energy status of the myocardium by shifting the heart's metabolic substrates from glucose to fatty acids, ketone bodies, and branched-chain amino acids in a non-diabetic porcine model of myocardial infarction [17]. This evidence concerns the gene SLC5A2 and myocardial infarction.