In this regard, the injection of apelin before MI enhanced PI3K-dependent potassium channel (IK1/Kir2.1) currents and reverted the ischaemia- and hypoxia-induced resting membrane potential depolarization and prolongation of QT interval on the ECG, which is thought to be the pro-arrhythmogenic mechanism following MI [107]. The gene discussed is APLN; the disease is myocardial infarction.