Haghika and Hazen et al. 59 reported that pseudo-germfree status exacerbates HFD-induced abnormal cholesterol metabolism and atherosclerosis in ApoE-/- mice and that a specific metabolite of intestinal bacteria, propionic acid, could improve cholesterol metabolism and atherosclerosis by decreasing the expression of NPC1L1 through an immune-dependent regulatory mechanism. The gene discussed is NPC1L1; the disease is atherosclerosis.