In addition, the western blot data demonstrated that the expression of ADH, which plays a role in the conversion of alcohol to acetaldehyde, was significantly inhibited in AF-treated Akr1a1−/− mice, but CYP2E1, which works alongside ADH in alcohol metabolism, was expressed at a relatively higher level in the AF-treated Akr1a1−/− group than in the other groups (Fig. 3K). This evidence concerns the gene CYP2E1 and atrial fibrillation.