Examples include variants in PRKAG2, GLA, ALPK3, CACNA1C, DES, FHL1, FLNC, GLA, LAMP2, PRKAG2, PTPN11, RAF1, RIT1, and TTR. Pathogenic variants in PRKAG2, encoding the gamma-2 regulatory subunit of adenosine monophosphate (AMP)-activated protein kinase (AMPK) [86], cause severe ventricular hypertrophy, electrocardiographic pre-excitation and conduction system disease [87]. This evidence concerns the gene GLA and cardiac hypertrophy.