Meanwhile, ALDH2, which plays an important role downstream of ADH and CYP2E1 by converting the resultant acetaldehydes to acetate in the mitochondria, was slightly increased in both AF-treated WT and Akr1a1−/− mice than those of their PF-treated counterparts, with a similar trend (Fig. 3K). This evidence concerns the gene AKR1A1 and atrial fibrillation.