For example, PTEN is mutated in >60% of primary brain tumors where deletion or inactivating mutations is a critical step for transformation to highest grade of astrocytoma GBM.30 Recent studies also demonstrate that PTEN protein can be transferred to PTEN-deficient tumor cells via paracrine mechanism31, 32 to inhibit cancer cell growth but the difficulty in re-expressing or delivering PTEN in tumor cells in an in vivo setting is a challenge that limits translation to the clinic. This evidence concerns the gene PTEN and glioblastoma.