EGFR and glioblastoma: Epidermal growth factor receptor amplification occurs at a much lower incidence in LUAD (~5%).10 Additionally, the EGFR mutations responsive to EGFR inhibitors are typically found in the intracellular tyrosine kinase domain.11 These EGFR mutations in LUAD result in a constitutively active form of the receptor protein which, in contrast to ECD missense mutations in GBM, are ligand-independent.