As downstream effectors of TAMs, M2-induced cytokine IL-10, as well as immunosuppressive factors B7-H4 and CSF1R, were increased correspondingly, which may inhibit the cytotoxic activity of tumor-associated antigen-specific T cells and promote lymphoma cell evasion.44–46 Our data demonstrated that the FBXW7-NOTCH-CCL2/CSF1 axis as an important mechanism of tumor progression provoked by TAMs in DLBCL. The gene discussed is VTCN1; the disease is neoplasm.