In PDAC, gut-derived LPS (≥500 pg/mL in the TME) exerts dual effects: via TLR4/MyD88/AKT/NF-κB signaling, it upregulates tumor PD-L1 to promote immune evasion, yet recruits CD3+CD8+ T cells for antitumor activity (80). The gene discussed is NFKB1; the disease is neoplasm.