A number of studies on zebrafish and mice that inhibited plasma membrane trafficking of TREK-1 by inactivating the interacting proteins POPDC1 and POPDC2 revealed exercise- and age-dependent sick sinus syndrome and atrioventricular block (78, 86), suggesting a role for TREK-1 in cardiac automaticity. The gene discussed is KCNK2; the disease is atrioventricular block.