In particular, activation of various oncological pathways, such as (a) the RET/PTC rearrangement in papillary thyroid carcinomas [30], (b) the human epithelial growth factor receptor HER-2 in breast cancer cells [31], (c) the Hypoxia inducible factor 1 (HIF-1), and (d) the vascular endothelial growth factor (VEGF) in glioblastoma [32] have all been shown to drive CXCR4 over-expression in cancer cells making them highly responsive to CXCL12 stimulation. Here, RET is linked to glioblastoma.