We showed here that in addition to reduced INa, iPSC-CMs from DMD patients also have reduced IK1 and probably alterations in other proteins altogether causing proarrhythmic alteration in electrical impulse conduction, likely because of trafficking disruption of the α1-syntrophin-mediated macromolecular complex formed by the DACP with Kir2.1and NaV1.5. The gene discussed is SCN5A; the disease is Duchenne muscular dystrophy.