In the contest of genetic disease, thickening of LV walls can results also by mutations in non sarcomeric proteins involving or the gene encoding the γ-2-regulatory subunit of the AMP-activated protein kinase (PRKAG2), or the gene encoding lysosome-associated membrane protein 2 (LAMP-2), resulting in Danon-type storage disease with clinical manifestations limited largely to the heart (usually with massive degrees of LV hypertrophy and ventricular pre-excitation) [9] (Figure 7). This evidence concerns the gene LAMP2 and hereditary disease.