Genes encoding for the sarcomeric β-myosin heavy chain (MYH7), the LMNA gene producing the nuclear lamina proteins lamin A and C, the desmin encoding gene (DES), ion channel coding genes (i.e., SCN5A), and many others were identified to be responsible for CDM, although at a lower prevalence compared to TTN. Gramlich et al., have developed an iPSC-based model system for DCM caused by truncating mutation in exon 326 of TTN. In their study, the authors demonstrated the beneficial effects of antisense oligonucleotides (AONs) exon skipping in the DCM phenotype. This evidence concerns the gene TTN and familial dilated cardiomyopathy.