Their direct interaction is essential to support tumor survival and growth [10] by at list three complementary pathways: (1) An autocrine effect on malignant cells that produce CCL2, and other CCR2 ligands, and also express their receptor (CCR2) [10]; (2) Attraction of bone marrow derived monocytic cells from the bone marrow to target tissues by chemotaxis, and then inducing their differentiation into macrophages [11], in particular tumor associated macrophages (TAMs) [12], [13], [14], and (3) pro-angiogenic effects on the endothelium that also expresses CCR2 [15]. Here, CCL2 is linked to neoplasm.