More than fifty per cent of EGFR-amplified GBM cases have in-frame deletions of exons 2–7 that code for the extracellular ligand-binding domain (EGFRvIII mutation) resulting in EGF-independent constitutive signaling and more aggressive tumor growth, higher invasiveness, increased resistance to treatment, and poor prognosis [60–62]. The gene discussed is EGF; the disease is glioblastoma.