Therefore, dysregulation of EGFR and/or hyperactivation of EGFR as a result of overexpression or mutation is tightly linked to pathogenesis of human cancers.2 Deletion of exons 2–7 of EGFR results in ligand-independent, constitutively active EGFR variant III, which is the most common EGFR mutation in glioblastoma.4 In addition, EGFR deletions in exon 19 and EGFR mutations such as L858R are found in lung cancer and are sensitive to the tyrosine kinase inhibitor gefitinib. The gene discussed is EGFR; the disease is glioblastoma.