Analyses of data from basic and clinical studies suggest that TAMs (activated M2 or alternative phenotype, tumorigenic), in contrast to classical M1 (resting MF phenotype, tumoricidal), express a number of cytokines/chemokines or decoy receptor molecules (e.g., dTNFR, IL-d1RA, dIL-1R, Eotaxin-2/CCL24, CCL18, CXC, IL-10, GFs, TGF-β, M-CSF, PGE2) that are immune suppressors and facilitate neoplasia, angiogenesis and tumor growth, and contribute to the epithelial-mesenchymal transition [3,15,20,22,39,42,47,50,57,85,92,93,94,95,96,97,98,99,100]. Here, CSF1 is linked to neoplasm.