Previous studies by Zhang et al. [38] showed that hepatic BMAL1 promotes DNL via insulin-mTORC2-AKT signaling during refeeding in mice, and that the protective action of BMAL1 against alcoholic liver disease in mice depends on its ability to couple carbohydrate response element binding protein (ChREBP)-induced DNL with PPARα-mediated fatty acid oxidation [29]. Here, AKT1 is linked to alcoholic liver diseases.