PRKAG2 and left ventricular hypertrophy: From studies in a transgenic mouse model (later correlated with different evidence from individuals with PRKAG2 variants), it was possible to observe that changes in AMPK activities were related to greater accumulations of cardiac glycogen and higher degrees of left ventricular hypertrophy, as well as atrioventricular conduction via alternative pathways with ventricular preexcitation and sinus node dysfunction due to annulus fibrosis infiltration by cytosolic vacuoles rich in glycogen-filled enlarged cardiomyocytes [15,16,17].