These observations, together with our findings showing that NPC1L1 dysfunctional mice (ezetimibe-administered Npc1l1WT mice and Npc1l1KO mice) have lower diet-induced VLDL/LDL-apoM-S1P, indicate that CETP and NPC1L1 play key roles in regulating VLDL/LDL-apoM-S1P in humans, particularly in patients with dyslipidemia. The gene discussed is APOM; the disease is metabolic syndrome.