These pathways are also altered in gliomas, as leading mutations in high-grade gliomas include EGFR amplification (in 27-36% of cases; Ohgaki and Kleihues, 2007) or mutations (18-31% of cases; Liu et al., 2005), deletion of PTEN, the inhibitor of AKT and mTOR (15-40% of cases; Tohma et al., 1998) and inactivation of NF1, a RAS inhibitor (18% of cases; The Cancer Genome Atlas Research Network, 2008). The gene discussed is AKT1; the disease is glioma.