In contrast, it is well-established that sensitivity to EGFR inhibition correlates with low PI3K/Akt activity, since hyperactivation of the PI3K/Akt pathway through phosphatase and tensin homolog (PTEN) mutation renders glioma cells resistant to EGFR inhibition and, conversely, inhibition of PI3K signaling using different compounds has been shown to sensitize glioma cells to EGFR inhibitors [6], [9]–[11]. The gene discussed is EGFR; the disease is glioma.