EGFR alterations, including amplification, point mutations, and vIII, confer similar drug sensitivities to EGFR inhibitors in patient-derived GBM cells [13], and EGFR amplification and EGFRvIII are retained in most recurrent GBMs (when present in primary tumors) [14], suggesting these alterations have similar functional driving effects in these tumors. The gene discussed is EGFR; the disease is glioblastoma.