Previously, Nr1h4-null mice have been observed to be characterized by a full spectrum of NAFLD pathologies, including steatosis, inflammation, fibrosis, and carcinogenesis (56), and a deficiency of Nr1h4 in mice has been established to be linked to increases in the levels of triglycerides and cholesterol, comparable to the lipid and lipoprotein metabolism profiles of FXR (57). This evidence concerns the gene NR1H4 and steatosis.