Along the course of our study, Kim et al showed that FGF19 ameliorates hepatic steatosis via DNMT3a‐mediated repression of lipogenesis.[33] The role of DNMT3A in this study appears to be contradictory to the inhibitory effect of DNMT3A on Klb and fatty oxidation we observed in our study. This evidence concerns the gene KLB and fatty liver disease.