While this approach does not correct the primary defect in DMD, namely sarcolemmal instability caused by loss of dystrophin, is does address the major secondary pathologies of failed regeneration and fibrosis; therefore, these findings will likely be broadly impactful for the treatment of both genetic and nongenetic muscle diseases that exhibit progressive fibrosis and failed regeneration. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.