In AMPKα2 knockout mice, pressureoverload-induced left ventricular hypertrophy and dysfunction were exacerbated,and the consequent upregulation of AMPKα1 did not fullycompensate for the impairment of cardiac function caused byAMPKα2 deletion; meanwhile, AMPKα2overexpression prevented the development of pressure overload-induced HF [23, 24].Alternatively, the specific deletion of AMPKα1 had no adverseeffect on pressure overload-induced heart function in mice, butAMPKα1 overexpression specifically activated the protein kinaseCζ/activating protein-1 (AP-1) signaling pathway [25]. This evidence concerns the gene PRKAA1 and hydrops fetalis.