It is established, since the earliest observations of human dystrophinopathy, as well as of some dystrophin-deficient animal models, such as canine models, that some muscles develop true fiber hypertrophy as a response to dystrophin deficiency [53], while others undergo atrophy and wasting since the early stages of disease. This evidence concerns the gene DMD and neuromuscular disease caused by qualitative or quantitative defects of dystrophin.