TMAO was verified extensively to induce vascular inflammatory, endothelial dysfunction, and foam cell formation by activating nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPK)-related pathways, leading to atherosclerosis (46), renal damage, and fibrosis (47), and it is considered to be an independent gut microbiota-derived risk factor for cardiovascular and renal disease. The gene discussed is NFKB1; the disease is endothelial dysfunction.