In atherosclerosis, lipopolysaccharide, a Gram-negative endotoxin and an exogenous ligand for TLR4, can induce the activation of TLR4-MyD88-NF-κB signaling, followed by the release of atherosclerosis-related inflammatory factors such as TNF-α, IL1β, IL6, and MCP-1, leading to the development and progression of atherosclerosis (26). The gene discussed is CCL2; the disease is atherosclerosis.