EGFR amplification in primary glioblastoma is often associated with the expression of EGFRvIII, a ligand-independent constitutively active mutant of EGFR, capable of persistently activating the phosphatidylinositol 3-kinase (PI3K)/v-akt murine thymoma viral oncogene homolog (AKT) signaling pathway that promotes the survival of glioma cells [2]. Here, EGFR is linked to glioblastoma.