TMAO can not only significantly accelerate the development of atherosclerosis in apolipoprotein E-deficient mice but also activate the mitogen-activated protein kinase and NF-κB signaling pathways in endothelial cells and smooth muscle cells, thereby triggering inflammatory reactions in vessels and causing increased accumulation of foam cells in the vascular wall and atherosclerosis (Zeisel and Warrier, 2017). The gene discussed is APOE; the disease is atherosclerosis.