In fact, many studies demonstrated that TMAO-induced NF-κB activation is a significant downstream process that upregulates monocyte adhesion through upregulation of cellular adhesion molecules such as VCAM-1, but also intercellular adhesion molecule 1 (ICAM-1) and E-selectin, and enhances endothelial dysfunction [14,15]. The gene discussed is NFKB1; the disease is endothelial dysfunction.