DMD and Duchenne muscular dystrophy: Importantly, levels of MYOM3 fragments were restored toward wild-type levels when dystrophin expression was restored by exon skipping in mdx mice and when α-sarcoglycan (SGCA) expression was induced in SGCA deficient mice, suggesting that the MYOM3 fragments is a potential therapy-responsive protein biomarker for DMD and other neuromuscular disorders.