It has been reported that lack of FGF15 (Fgf15−/− mice) results in increased hepatic steatosis and the development of endoplasmic reticulum stress in the liver of mice fed a high fat diet; and in the same study, Alvarez-Sola et al. demonstrated how Fibapo treatment (a chimeric molecule based on the fusion of FGF19 with apolipoprotein A-I) protects from lipid-mediated cellular stress and damage in obese db/db mice undergoing partial hepatectomy without I/R [38]. This evidence concerns the gene APOA1 and steatosis.