We explored isoforms of dystrophin expressed by hiPSC-derived cardiac fibroblasts (hiPSC-fibs) obtained from control and DMD patients with out of frame deletions of exons (DMD1 and DMD4) and a patient who has a spontaneous point mutation in intron 47 (DMD5) that leads to a frameshift and the formation of a premature stop signal [13–15]. This evidence concerns the gene DMD and Duchenne muscular dystrophy.