DMD and Duchenne muscular dystrophy: ABE could correct nonsense point mutations in mouse models of DMD, and one study used CRISPR–Cas9 to construct DMD human iPSC cells with a large deletion in exons 48–54 (ΔE48–54), which disrupted myotonic dystrophin expression in cardiomyocytes derived from DMD human iPSCs, and subsequently, the study used ABE to convert AG to GG (35.9 ± 5.7%), skipping exon 55, restored myotonic dystrophin expression, suggesting that ABE‐mediated exon skipping has the potential to be used as a gene therapy for DMD.358