In detail, DCM phenotypes from structural changes and impaired mechanotransduction are observed secondary to pathogenic variants in a number of cytoskeletal genes, including TTN (titin), FLNC (filamin C), DES (desmin), DMD (dystrophin), LDB3 (ZASP protein), BAG3 (BCL2-associated athanogene 3), and the same desmosomal genes involved in ACM pathophysiology [61,62,63,64,65,66]. This evidence concerns the gene DMD and familial dilated cardiomyopathy.