Current classification systems recognize distinct molecular subtypes: mesenchymal, classical, and proneural, defined by characteristic mutations such as neurofibromatosis type 1 (NF1), phosphatase and tensin homolog (PTEN), and tumor protein 53 (TP53) in mesenchymal GBM; epidermal growth factor receptor (EGFR) amplification in classical GBM; and TP53, isocitrate dehydrogenase 1 (IDH1), and platelet-derived growth factor receptor alpha (PDGFRA) mutations in proneural tumors [2]. This evidence concerns the gene EGFR and glioblastoma.