Apart from this, EGFR variant III (EGFRvIII), a tumor-specific deletion of exons 2-7 which occurs in approximately 30% of GBM patients, consistently activates the EGFR signal even without ligands binding, contributing to intra-tumoral heterogeneity and resistance to targeted therapies (5–7). The gene discussed is EGFR; the disease is glioblastoma.