Intrathecal blockade of CXCL12/CXCR4 axis decreased the release of inflammatory cytokines, and attenuated ischemia‐reperfusion–induced inflammatory pain, which may be attributed to the inhibition of glial TLR4 activation in the spinal cord.10 CXCL12/CXCR4 signaling is involved in the development and maintenance of bone cancer pain via sensitizing neurons or activating astrocytes and microglia.11 CXCL12/CXCR4 axis also plays an important role in the neuropathic pain caused by peripheral nerve injury. This evidence concerns the gene CXCR4 and bone cancer.