Activation of PI3K signaling through the loss of PTEN or via overexpression of AKT has also been shown to promote GBM tumorigenesis in engineered mouse models and primary human cell systems [15]–[17], thus validating the clinical relevance of alterations in this pathway that have been found in GBM patients [18], [19]. The gene discussed is AKT1; the disease is glioblastoma.