MYD88 and neoplasm: This tissue-specific duality extends to other malignancies: in PDAC, LPS-TLR4/MyD88/AKT/NF-κB signaling upregulates tumor PD-L1 (80); in lung cancer with chronic Pseudomonas aeruginosa infection, LPS sustains TLR4-dependent chronic inflammation, recruiting MDSCs and amplifying PD-1/PD-L1 to impair checkpoint blockade (247).