KCNK2 and sick sinus syndrome: Finally, cardiomyocyte-specific K2P2.1 (TREK-1) knockout mice exhibit a phenotype of stress-induced sick sinus syndrome and prolongation of QT intervals that could be reproduced in a transgenic model which employed C-terminal truncation of beta IV spectrin to disrupt its interaction with K2P2.1 (TREK-1), thereby impairing intracellular K2P2.1 (TREK-1) protein trafficking [27,151].