In a chronic inflammatory state, some inflammatory mediators such as tumor necrosis factor (TNF), interleukin (IL)-1, and IL-6 can cause endothelial cell dysfunction and increased protein levels of adhesion molecules and chemokines on endothelial cell surface [22–25], thus contributing to the recruitment of monocytes into the arterial wall composed of endothelial cells; meanwhile, macrophages express scavenger receptors to promote the formation of foam cells, ultimately leading to the occurrence and development of atherosclerosis [26]. This evidence concerns the gene TNF and atherosclerosis.