Since cardiomyopathy development is also an important feature of the pathology observed in DMD patients [2], [3], as well as in DMD mouse models (e.g. [16]–[18]), reduced Nav1.5 currents and/or impaired Nav1.5 channel gating in dystrophic cardiomyocytes [7], [10] may be causally involved in the formation of dystrophic cardiomyopathy. Here, SCN5A is linked to Duchenne muscular dystrophy.