NO has a critical role in maintaining capillarization in tissues16, and because an SGLT2 inhibitor was reported to increase the phospho-AKT level in cardiac tissues of an ischemia–reperfusion injury model17 and activate AKT/eNOS signaling in HUVECs18, we speculated that EMPA treatment might activate AKT/eNOS signaling in the heart and attenuate capillary rarefaction in cardiac tissues, thereby improving systolic dysfunction after TAC. The gene discussed is AKT1; the disease is ischemia.