During pregnancy, maternal obesity profoundly influences the risk of obesity and metabolic diseases in the offspring; for example, the offspring of mothers fed an HFD (45% fat) for 12 weeks showed a non-alcoholic steatohepatitis phenotype (most prominent in males) and altered methylation patterns (hypermethylation) in genes implicated in liver fibrosis and lipid accumulation, such as Ephb2 (ephrin type-B receptor 2) and Fgf21 (fibroblast growth factor 21), suggesting that epigenetic changes could favour the development of fatty liver disease in the offspring [42]. The gene discussed is FGF21; the disease is obesity due to melanocortin 4 receptor deficiency.