In the TME, TAMs exhibit significant phenotypic plasticity, polarizing into either pro‐inflammatory M1‐like macrophages or pro‐tumorigenic M2‐like macrophages.[22] Based on our findings, we hypothesized that TNTs‐mediated material transfer could drive macrophages toward a tumor‐promoting TREM2+ phenotype, a subtype associated with immunosuppression and tumor promotion. The gene discussed is TREM2; the disease is neoplasm.