Complex formation has been evidenced to drive JAK-STAT-dependent transendothelial migration of tumor cells [107], the recruitment of neutrophils and macrophages into the TME through endothelial cell secretion of monocyte chemoattractant protein-1 (MCP-1) [108], M2 polarization of macrophages, inhibition of DC activation, and Treg differentiation [109]. This evidence concerns the gene CCL2 and neoplasm.