It is clear that GBM cell proliferation, migration, and invasion can be achieved through multiple signalling cascades, activated by kinase activity of wild-type EGFR, EGFRvIII, or both, highlighting the multifarious nature of EGFR signalling in GBM, which makes targeting EGFR as an anti-tumour strategy challenging for translation into clinical benefit. Here, EGFR is linked to glioblastoma.