,11,12 Single or multiple exonic deletions and duplications account for 80% of the mutations that cause DMD and BMD, and the “reading-frame rule” can explain more than 90% of the mutations in DMD. 13Previous studies on the pathomechanism of dystrophin-associated DCM using patient-derived or genome-edited human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) recapitulated aberrant cell physiology, including abnormalities in contraction, calcium handling, and mitochondrial dysfunction.14 This evidence concerns the gene DMD and familial dilated cardiomyopathy.