Between 40 and 50 % of glioblastoma multiforme (GBM) cases carry alterations of the EGFR, and approximately half of these co-express the mutated variant EGFRvIII, which has a deletion of exons 2–7 that generates a constitutively active receptor, even in the absence of ligand binding [2]. This evidence concerns the gene EGFR and glioblastoma.