Indeed, the fact that targeting this pathway seems to have no considerable or long term benefits either in solid tumors or metastatic cancers suggest that other compensatory mechanisms may be involved; whether this is due to increased CCL2, upregulation of CCR2, or contribution by other functionally analogous chemokines and/or chemokine receptors is yet to be delineated. This evidence concerns the gene CCR2 and metastatic malignant neoplasm.