Compared with other models the degree of liver injury was intermediate; this, together with the fact that steatohepatitis developed in only half of the mice, should be considered as a strength of our study because it allows an assessment of inhibition as well as stimulation of liver steatosis and inflammation by additional interventions, such as the genetic knockout of Ebi2, Cyp7b1, or Ch25h. HFD feeding models such as ours with high caloric intake, rich in cholesterol, saturated fats, and fructose are time-consuming but adequately reflect the human condition. This evidence concerns the gene CH25H and Hepatic steatosis.