In addition to mutations in desmosomal genes, an increasing number of non-desmosomal genes, such as desmin (DES), titin (TTN), lamin A/C (LMNA), Phospholamban (PLN), Transmembrane Protein 43 (TMEM43), and the sodium channel Nav1.5 (SCN5A) have also been reported as causative genes for ACM by using candidate gene sequence methods and linkage analysis, as inherited mutations identified in humans with cardiomyopathy are now modeled in transgenic or knock-in animals [46, 47]. This evidence concerns the gene DES and cardiomyopathy.