Our electrophysiological studies revealed that Fontan operation resulted in complex ionic remodeling caused by the aberrant expression of ionic channels, including Kv4.3/KCND3 (Ito), Kir2.1/KCNJ2 (IK1), Cav1.2/CACNA1C (ICa,L), and SCN5A (INa), which might account for the net shortening of AERP and APD in the post-Fontan atrium as an important arrhythmogenic substrate for atrial tachycardia. Here, KCNJ2 is linked to atrial tachycardia.