Critically, LPS also reprograms tissue-resident CD14+CD8+ T cells—enriched in TILs of TLR4-competent patients, exhibit higher granzyme B production than CD14-CD8+ T cells upon LPS-TLR4 engagement (133), and their depletion abrogates LPS-induced tumor regression in syngeneic B16 melanoma models, confirming a causal role in effector function. The gene discussed is CD14; the disease is neoplasm.