[19] that found whole body PTP1B deletion improved cardiomyocyte contractility in mice fed HFD, through an AMPK-dependent mechanism. Furthermore, myeloid-specific deletion of AMPKα1 on an LDLR−/− mouse background, resulted in hypercholesterolemia, increased macrophage inflammation and plaque infiltration and exacerbated atherogenesis [20]. This evidence concerns the gene PRKAA1 and familial hypercholesterolemia.