Our observation that CXCL12- and PDGFBB-induced chemotaxis are both abolished by intracellular Ca2+ chelation while not affected by inhibition of c-src, src-like kinases and c-Abl, further suggests common intracellular pathways, strengthening the hypothesis that in glioblastoma CXCR4 and PDGFR are co-activated during single receptor stimulation and cooperate sharing intracellular signaling mechanisms. This evidence concerns the gene CXCR4 and glioblastoma.