Research to date has shown that DRG neurons express receptors (CC chemokine receptor 2 and 4) activated by MCP-1 [46], and that lack of CCR2 receptor can impair inflammatory and neuropathic pain responses [47,48]; all supporting a potential role for MCP-1 for the unique type of pain elicited at the site of bone cancers. Here, CCL2 is linked to bone neoplasm.