DMD and neuromuscular disease caused by qualitative or quantitative defects of dystrophin: The calcium hypothesis of dystrophinopathy assumes that abnormal Ca2+‐handling and impaired cellular signalling events at the level of the sarcolemma, transverse tubules, triad junctions, the luminal sarcoplasmic reticulum and the sarcosol are responsible for increased Ca2+‐dependent muscle protein degradation in dystrophin‐deficient skeletal muscle fibres [38].