These findings suggest a strong possibility that, in addition to the main pathological role of dystrophin in DMD (i.e., muscle damage due to the reduction or deficiency of dystrophin by mutations), abnormal Ca2+-buffering by CASQ1 and/or CASQ-like proteins in the SR, in combination with excessive SOCE, could be related to the pathological mechanism of DMD. This evidence concerns the gene DMD and Duchenne muscular dystrophy.