Phosphatidylinositol-3-kinase (PI3K)/Akt (protein kinase B) signaling is aberrantly activated in glioblastomas and other tumors, often due to mutation or loss of the Phosphatase and Tensin homolog (PTEN) antagonizing class I PI3K signaling, or to amplification or overexpression of growth factor receptors acting upstream of class I PI3K [4], [5]. This evidence concerns the gene PTEN and glioblastoma.