Recent studies have shown that cardiomyocytes from DCM patients often exhibit abnormal sarcomeric structure, which is likely due to pathogenic mutations in sarcomere protein-coding genes such as giant sarcomere protein titin (TTN), cardiac troponin T (TNNT2), tropomyosin 1 (TPM1), and desmin (DES; Fürst et al., 1988; Sehnert et al., 2002; Deacon et al., 2019). This evidence concerns the gene DES and familial dilated cardiomyopathy.