Under such conditions, the significance of ClC-2 in the heart is deemed to become more prominent, and there is also a possibility that ClC-2 participates in these pathological processes, particularly the associated arrhythmogenesis as a result of abnormal membrane depolarization, enhanced automaticity generating ectopic excitations, or excessive shortening of the action potential duration occurring in acute myocardial ischemia. This evidence concerns the gene CLCN2 and myocardial ischemia.