Because food intake or body length did not significantly alter between Wdr76−/− and Wdr76+/+, it is possible that decreased body weight and hepatic steatosis phenotypes in HFD-fed Wdr76−/− mice could be attributed to improved insulin sensitivity, altered glucose and lipid metabolism, or enhanced energy consumption etc. In addition, we also consider the possibility that deficiency of WDR76 in liver tissue could prevent fatty liver and improve lipid metabolism due to whole-body Wdr76 knockout mice. The gene discussed is WDR76; the disease is fatty liver disease.