In the present study, both the sarcolemmal Kv1.4/Kv4.2 were markedly reduced in EtOH-treated ALDH2*2 KI mice compared to those of their respective EtOH-treated Wt mice, indicating a critical dysfunction in Ito and repolarization processes from ALDH2 enzyme deficiency exposed to EtOH that may facilitate arrhythmia substrate formation. This evidence concerns the gene ALDH2 and Arrhythmia.