Studies on iPSC-CM models of HCM mostly involve sarcomere mutations, with MYH7 being the most prevalent (6/13), coding for myosin heavy chain-β, followed by MYBPC3 (2/13), coding for cardiac myosin-binding protein C, ACTC1 (2/13), coding for α-actin and TNNT2 (1/13), encoding cardiac troponin T. Metabolic disorders with the HCM phenotype included several storage-related diseases, such as the lysosomal storage disease Fabry disease, caused by a mutation in the α-galactosidase A gene [11]. This evidence concerns the gene MYBPC3 and lysosomal storage disease.