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. The gene discussed is NF1; the disease is glioblastoma.