Several genetic alterations are recurrently implicated in primary GBM, among which PTEN inactivation is the most frequent, shown to occur through different mechanisms [6, 7]. PTEN loss of function (LOF) promotes an increased PI3K signalling [8, 9] which activates, among others, the atypical Protein Kinase C (aPKC) [10, 11], resulting in alterations in tissue morphology both in Drosophila [12] and in mammalian cells [13]. This evidence concerns the gene PTEN and glioblastoma.