With regard to limitations of our study, we cannot exclude the possibility that pathways other than hepatic gluconeogenesis — such as glycogenolysis, glycolysis, and glucose cycling in the liver as well as glucose uptake in extrahepatic organs — may contribute to the improved glucose metabolism induced by hepatic FASN deficiency in the mouse obesity models. Here, FASN is linked to obesity due to melanocortin 4 receptor deficiency.