Moreover, LPS–TLR4 signaling in breast-cancer cells can activate NF-κB and pro-invasive programs, while TAM-derived IL-10 sustains immunosuppression—motivating co-profiling of metabolites and MAMP pathways (e.g., TLR4 activity) when interpreting immune phenotypes or designing combinations [218]. The gene discussed is TLR4; the disease is breast carcinoma.