This mechanism was also suggested in a trial investigating gefitinib, which showed a significantly better PFS and OS in patients with de novo GBM with EGFR gene alterations combined with wildtype phosphatase and tensin homolog (PTEN) (inactivation of the AKT pathway) compared to patients with wildtype EGFR and altered PTEN (activation of the AKT pathway) [33]. This evidence concerns the gene AKT1 and glioblastoma.