AKT1 and central nervous system cancer: H2O2-dependent increases in PIP3 abundance and Akt activity were correlated with the oxidative inactivation of PTEN in PTEN-expressing glioma cells, but not in PTEN-null glioma cells, further supporting the notion that oxidative stress regulates PI3K-dependent signaling through the oxidative inhibition of PTEN [[43], [44], [45]].