Using the dystrophin-deficient mdx mouse model for human DMD (3), we and others previously reported that the lack of dystrophin causes a significant peak Na+ current (INa) loss both in ventricular cardiomyocytes of the working myocardium (4–6) and in Purkinje fibers (7, 8), ventricular myocytes specialized for rapid electrical impulse conduction. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.