If the dystrophin/utrophin double mutant mouse is indeed a suitable model for DMD with representative cardiac pathology (probably superior to the mdx mouse), as suggested by several groups (e.g. [16], [19], [20]), our finding of a more severe cardiac sodium channel dysfunction in this mouse model has an important implication: sodium channel impairments may be considered a major cause of the cardiac conduction defects observed in DMD patients [11], [12], probably as yet underestimated when using the common mdx mouse as model system. This evidence concerns the gene DMD and Duchenne muscular dystrophy.