Thus, chemokine CXCL12 through the autocrine/paracrine activation of its receptor, CXCR4, also proposed as surface marker for GBM CSCs [35], may represent a valuable target to block GBM CSCs self-renewal [36], or their invasive behavior [37], using CXCR4 antagonists such as the clinically approved drug Plerixafor (AMD3100) [38], or novel compounds recently described [39]. This evidence concerns the gene CXCR4 and glioblastoma.