Together, these data show that inhibition of DMD-exo secretion resulted in cytoprotection for DMD-iCMs (Fig. 2) and an anti-fibrotic action in stressed mdx mouse hearts (Fig. 3); therefore, long-term exposure to DMD diseased exosomes is implicated in the pathological processes contributing to the development of cardiomyopathy. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.