A cardiac-specific knockout of Kcnk2 encoding TREK-1 displays a stress-induced sinus bradycardia similar to the one observed in Popdc1 and Popdc2 null mutants [68], which means that the sinus bradycardia phenotype of POPDC mutants could at least be partially explained by the loss of the POPDC-TREK-1 interaction. This evidence concerns the gene KCNK2 and Sinus bradycardia.