CCL2-dependent recruitment of inflammatory monocytes (Ly6ChiCD11b+CD11c–MHCII–VCAM1–CCR2+) to the cancer site and their exposure to M-CSF and other tumor-derived factors leads to the generation of tumor-associated macrophages (TAM) that demonstrate self-renewal capacity [29,33] Both MDSC and TAM are key players in cancer progression and will be discussed in this review. This evidence concerns the gene CCL2 and neoplasm.