Considering the aberrant expression of IRF3 in human lung cancer and the crucial role of NF-kB activity in lung cancer carcinogenesis [59, 60], the mechanisms underlie TLR4-induced IL-33 expression in NSCLC cells might involve IRF3 and NF-kB pathway, as well as HMGB1 since it binds to LPS to facilitate LPS transfer and initiate TLR4 signaling [61]. The gene discussed is IRF3; the disease is lung cancer.