Furthermore, analysis of apolipoprotein profiles from the blood of Ces1g deficient mice showed protein composition changes, including increased apoE and apoCIII (an endogenous inhibitor of lipoprotein lipase (LpL)) and decreased apoCII levels (an endogenous activator of LpL), which can cause blunted blood apoB-containing lipoprotein clearance and contribute to the observed hyperlipidemia. The gene discussed is LPL; the disease is hyperlipidemia.