Once activated by CCL2, MAMs produce the autocrine chemokine CCL3, which enhances the interaction between vascular cell adhesion molecule-1 (VCAM-1) on tumor cells and the α4 integrin on MAMs, resulting in a reciprocal, efficient retention and extravasation of macrophages and CTCs at the metastatic site, as demonstrated in various spontaneous and transplantable murine cancer models [116]. This evidence concerns the gene VCAM1 and neoplasm.