EGFR and glioblastoma: The most common structural variant in GBM, EGFR variant III (EGFRvIII), is characterized by a truncated extracellular domain lacking the ligand-binding site and is constitutively active and highly oncogenic.3 Altered signaling via EGFR and/or EGFRvIII is involved in GBM proliferation and invasion.4 At the molecular level, EGFR and EGFRvIII interplay5 or interact with other RTKs6,7 to fine-tune these oncogenic processes.