In tumor-infiltrating macrophages, LPS/TLR4 signaling sustains NF-κB -driven IL-10 production and dampens effector T-cell activity, while intratumoral bacteria are prevalent (including in lung cancers) and correlate with immunotherapy response—highlighting a pattern-bound axis that can oppose or re-shape metabolite effects [39, 214, 215]. The gene discussed is NFKB1; the disease is neoplasm.