EGFR amplification is often associated with high expression of EGFRvIII, a ligand-independent constitutively active mutant of EGFR, capable of persistently activating PI3K/v-Akt murine thymoma viral oncogene homolog (Akt) signaling pathway that promotes the survival of the glioma cells. The gene discussed is AKT1; the disease is central nervous system cancer.