Additionally, GBM has been described to exhibit mutations, translocations, deletions, and amplifications involved in the downregulation of phosphatase and tensin homolog (PTEN) [6], F-box, WD40 domain protein 7 (FBXW7) [7], neurofibromatosis1 (NF1), p14 alternative reading frame (ARF), tuberous sclerosis proteins 1⁄2 (TSC1/2), Von Hippel–Lindau protein (pVHL) [8], liver kinase B (LKB1) [9], and anti-apoptotic proteins such as Bax, Bad, and the apoptotic protease activating factor-1 (Apaf-1), caspase-8, and caspase-7 [10,11,12,13]. This evidence concerns the gene PTEN and glioblastoma.