In particular, the protective effects of AMPKα2, which ishighly expressed in the heart, in HF include promoting the remodeling of energymetabolism, improving mitochondrial dysfunction, activating mitochondrialautophagy, attenuating oxidative stress, and reducing cardiomyocyte death.Therefore, targeted therapy against AMPKα2 may achieve betterresults in treating HF. The gene discussed is PRKAA2; the disease is hydrops fetalis.