Mechanistically, we found that Escherichia-Shigella- and unclassified_f__Enterobacteriaceae-derived LPS activated the TLR4-mTOR-NF-κB-IL-6 axis to facilitate NSCLC cell proliferation, whereas rapamycin effectively delayed LPS-induced tumor cell proliferation in vitro and in vivo functional experiments. The gene discussed is NFKB1; the disease is neoplasm.