EGFRvIII, the dominant mutation occurring in around 30% of GBM patients, is characterized by the deletion of EGFR exons 2–7, resulting in a removal of amino acids 6–273 from the extracellular ligand-binding domain and inserting a glycine residue not found within the reading frame of wild type EGFR, thus creating a novel junction between exons 1 and 8 [31]. Here, EGFR is linked to glioblastoma.