However, our study suggests that the observed antitumor response after TLR/MyD88/NF-κB pathway inhibition is mediated by a delicate balance between immune activation and immune suppression in the tumor microenvironment (TME), It provides a baseline for the development of alternative intervention modalities., and paves the way for the introduction of agents inhibiting innate immune signals such as TLRs for prevention and treatment of K-ras mutant lung cancer in high-risk individuals (Smokers with and without COPD). The gene discussed is NFKB1; the disease is neoplasm.