Respectively, our lab recently developed an in vitro cellular disease model for DMD by reprogramming dystrophic mouse fibroblasts into iMPCs that did not express the dystrophin protein, enabling to assess dystrophin restoration by CRISPR-Cas9.[75] We envision that derivation of mouse iSMCs or human SMCs from DMD myogenic cells may provide an optimized in vitro model for basic research applications, or as a platform to test therapeutic interventions that may prove beneficial for DMD patients. This evidence concerns the gene DMD and Duchenne muscular dystrophy.