Proteogenomic and cell-based analyses of GBM showed PTEN inactivation in 51% of primary glioblastomas of all transcriptional subtypes, conferring increased metabolic flux and apoptosis resistance through activation of the phosphatidylinositol-3′-kinase (PI3K)-Akt pathway (3–6). The gene discussed is AKT1; the disease is glioblastoma.