Julian N. Ramos et al. engineered eight dystrophin truncations that achieved uniform skeletal muscle expression but exhibited differential efficacy in nNOS expression and force recovery [74]; concurrently, Cora C. Hart et al. demonstrated that four clinical-stage microdystrophin constructs rescued hereditary myopathy in mdx mice, while two variants paradoxically induced cardiomyopathy characterized by impaired cardiac contractility and exacerbated myocardial fibrosis [83]. This evidence concerns the gene DMD and cardiomyopathy.