Studies in prostate cancer models show that the exposure of PC3 cells, derived from bone metastases, to increasing concentrations of CXCL12 leads to an up-regulation of the CXCR4 gene, and this mechanism is mediated by NF-kB: this results in increased adhesion (175–200%) and the trans-endothelium migration of cancer cells. Here, CXCR4 is linked to cancer.