The chronic inflammation stimulated by the excessive penetration of LPS into circulation has been considered as one of the important factor [55], and the mechanism may be that LPS can activate Toll-like receptor 4 expressed in various vascular cells and perivascular adipose tissue, stimulate the release of proinflammatory cytokines, inhibit cholesterol efflux from macrophages, facilitate foam cell formation, and exacerbate atherosclerosis [55,56]. The gene discussed is TLR4; the disease is atherosclerosis.