In order to test the hypothesis that the DAPC is important in the regulation of Kir2.x channels, here we have studied potential IK1 abnormalities in dystrophin-deficient ventricular cardiomyocytes derived from DMD mouse models. Besides the classical dystrophin-deficient mdx mouse,23 we also used mice additionally carrying a mutation in the utrophin gene (mdx-utr).24,25 The latter DMD mouse model develops a more severe cardiomyopathy with an earlier onset compared to mdx.25,26