Data from the bmx mouse presented here demonstrate that even if dystrophin restoration from exon skipping treatment achieves 100% efficacy, the resultant ‘Becker‐like’ dystrophin may be expressed at lower‐than‐normal levels in muscle due to other factors, and therefore pathology including muscle damage, inflammation, weakness and cardiomyopathy will persist. This evidence concerns the gene DMD and cardiomyopathy.