CCL2 and neoplasm: Molecular interactions with pattern receptors (e.g., TLR4 and downstream MYD88), and immunosuppressive signals mediated by engagement with cell surface inhibitory molecules (e.g., TIGIT) or elaboration of suppressive cytokines (e.g., VEGF and CCL2) result in immune evasion that likely contributes to ineffective immunosurveillance of nascent, developing and established neoplasia.