Particularly, chemokine (C–C) ligand 18 (CCL18) is highly expressed in TAMs and promotes the invasion and metastasis of cancer cells by triggering integrin clustering and enhancing their adherence to the ECM, a phenomenon mediated by the receptor membrane-associated phosphatidylinositol transfer domain-containing proteins (PITPNM3).42 Therapeutic success in minimizing the protumoral roles of TAMs in animal models and in early clinical trials suggests that TAMs are attractive targets to prevent resistance as part of combination therapy in cancer treatment.43 This evidence concerns the gene CCL18 and cancer.