Since previous studies have demonstrated that ablating BCO1 resulted in over-expression of BCO2 [29,30], we used the BCO1/BCO2 double knock out (DKO) mouse model and demonstrated that BCO1/BCO2 DKO mice developed hepatic steatosis and had significantly higher levels of hepatic and plasma triglycerides and total cholesterol compared to wild type (WT) mice with fully functioning BCO1 and BCO2 [32]. The gene discussed is BCO1; the disease is Hepatic steatosis.