Aberrant growth factor signaling through receptor tyrosine kinases (RTKs) is a hallmark of cancer, and triggers abnormal cell proliferation, enhanced motility, and therapeutic resistance of many solid tumors including glioblastoma (GBM).1 The Cancer Genome Atlas (TCGA) project confirmed alterations in RTK genes or downstream pathways as essential drivers of GBM, detectable in >80% of patients.2 In particular, the epidermal growth factor receptor (EGFR) is predominantly amplified/mutated. This evidence concerns the gene EGFR and glioblastoma.