A clue that autophagy was defective in DMD was provided as early as in 2011, when Eghtesad and colleagues showed that the administration of rapamycin, an inhibitor of mammalian target of rapamycin (mTOR) and a stimulator of autophagy, ameliorated the dystrophic phenotype in mdx mice by reducing the infiltration of T cells within the muscle fibers and the ensuing necrosis [62]. This evidence concerns the gene MTOR and Duchenne muscular dystrophy.