CMR studies indicate that fibrosis is involved in myocardial involvement in dystrophinopathies [13–16]; this appears to be a consequence of the same mechanisms observed in skeletal muscles [25]: Cardiomyocyte membranes are disrupted owing to the lack of dystrophin and a subsequent increase in intracellular concentration of calcium [26]. Here, DMD is linked to neuromuscular disease caused by qualitative or quantitative defects of dystrophin.