A recently published review article12 deals with protein assemblies of cardiac Nav1.5 sodium and inward rectifier Kir2.1 potassium channels, that control cardiac excitability and, in case of dysregulation, introduce arrhythmogenesis. Interestingly, these 2 channels not only share a number of common protein interaction partners (e.g., caveolin-3, synapse-associated protein-97, and syntrophin) (12 and references therein), but also modulate each other's cell-surface expression.14,18 These findings suggest organization of Nav1.5 and Kir2.1 in one or several common protein complexes. Here the DAPC stands out as a likely candidate. Thus, at the cardiomyocyte membrane, both channels interact through the PDZ domain-scaffolding protein syntrophin (see Fig. 2A in12), which is a direct binding partner of dystrophin within the DAPC.