AMPKα2 deficiency was shown to enhance myocardial ischemia/reperfusion injury in a mouse model with cardiomyocyte-specific overexpression of a mutant AMPKα2 catalytic subunit [83], and to exacerbate pressure overload induced left ventricular hypertrophy and dysfunction in AMPKα2 knock-out mice [84]. This evidence concerns the gene PRKAA2 and left ventricular hypertrophy.