Amplification of the EGFR gene (with a frequency of ∼50% in glioblastoma multiforme-GBM) (Furnari et al., 2007) is often associated with a tumor-specific mutation encoding a truncated form of the receptor, which lacks the extracellular binding domain, known as ΔEGFR (also named de2-7EGFR or EGFRvIII) leading to ligand-independent, constitutive tyrosine kinase activity. This evidence concerns the gene EGFR and glioblastoma.