This hypothesis was generated based on the following data: (i) H2O2 treatment enhances the phosphorylation of AKT in GBM cells [23]; (ii) the PI3K/AKT signaling pathway is associated with GBM development and the deregulation of elements related to this cascade results in uncontrolled tumor growth [24,25]; PI3K inhibitors are currently in clinical trials as anti-glioblastoma therapeutics [26]; and (iii) GAB decreases the phosphorylation level of AKT in HCC cells transfected with GLS2 [17]. The gene discussed is AKT1; the disease is glioblastoma.