Several lines of evidence led to the concept that the CXCL12/CXCR4 axis is a key effector of the nonrandom typical invasive pattern of human GBM [9]: the overexpression of CXCR4 in the invasive GBM cells [4]; the in vivo localization of CXCR4 in the hypoxic areas [10], considered the basis for the acquisition of a highly invasive phenotype [11]; the demonstration that CXCR4 expression is under the control of HIF1 and VEGF [12]. Here, CXCR4 is linked to glioblastoma.