In this study, we used several colonies of genetically mutated mice with different background. Alcohol-induced fatty liver in mice may be susceptible to genetic background. Therefore, the comparison was made among those mice with the same genetic background, and the comparison between those mice with different background was avoided. For example, Pparα+/+/Cyp2a5−/− mice and Pparα−/−/Cyp2a5−/− mice were litter mates sharing the same background, thus, the comparison between them leads to a conclusion that the enhanced alcoholic fatty liver in the Cyp2a5−/− mice is due to the failed upregulation of the PPARα-FGF21 axis by ethanol in Cyp2a5−/− mice. However, due to the different background, Fgf21alb-cre mice and Fr1alb-cre mice are not comparable. Although liver TG levels and steatosis scores were statistically higher in Fgf21alb-cre mice than in Fr1alb-cre mice (Fig. 5C, 5D), a conclusion that liver FGF21 plays a more important role in alcoholic fatty liver than liver FR1 was not from a direct comparison between Fgf21alb-cre mice and Fr1alb-cre mice. Instead, by comparing Fgf21alb-cre mice and Fgf21fl/fl mice, we know that liver FGF21 plays an important role in alcoholic fatty
