Apart from the well described regulation of Nav1.5 sodium channels by the DAPC in cardiomyocytes, evidence has been accumulating that this protein complex also plays a role in regulating Kir2.x inward rectifier potassium channels. Thus, like Nav1.5, Kir2.x channels do interact with the DAPC protein syntrophin through their PDZ-binding motifs.12,16,17 Moreover, Nav1.5 and Kir2.1 colocalize and modulate each other's surface expression in cardiomyocytes,14,18 suggesting organization of these 2 channels in a common protein complex. Based on this evidence, the authors of a recently published review article12 hypothesized that the DAPC is important in the regulation of Kir2.x channel expression and function. Functional evidence for this hypothesis, however, has been lacking so far. Kir2.x channels in ventricular cardiomyocytes (most prominently Kir2.119,20) account for the inward rectifier potassium current IK1, which controls the resting membrane potential, and the final phase of action potential repolarization.19,21 Clinically, mutations in the KCNJ2 gene encoding for Kir2.1 induce diseases associated with severe cardiac arrhythmias and increased risk of sudden cardiac death.21,22