IDH1 and glioblastoma: The patient's overall molecular pathology was largely consistent with the ‘classical GBM’ subtype proposed by Verhaak, et al. [32], which is characterized by EGFR amplification and a lack of abnormalities in TP53, NF1, PDGFRα, and IDH1. It is possible that EGFR amplification and EGFRvIII positivity could underlie the encouraging response to afatinib plus temozolomide.