EGFR and glioblastoma: We were initially surprised that the CTX resistant cells showed sustained high levels of total and activated EGFR despite the low affinity for EGF, though these results mirror previous reports of ECD missense mutations—albeit in glioblastoma—which showed constitutive EGFR activity in the absence of EGF suggesting that ECD mutations can have tumorigenic receptor-activating potential [7, 52, 53].