LPS binding to TLR4 leads to NF‐κB activation and expression of proinflammatory cytokines, such as IL‐1β, TNF‐α, and IL‐6; generates an inflammatory microenvironment; recruits neutrophils; releases the Ser proteases, neutrophil elastase (NE), and cathepsin G; induces antitumorigenic factor thrombospondin‐1 protein degradation; and enhances tumor cell lung metastasis.225. The gene discussed is TLR4; the disease is neoplasm.