The majority of primary GBM is characterized by IDH wild-type genotype, telomerase reverse transcriptase (TERT) mutations [4], epidermal growth factor receptor (EGFR) amplification [8], alterations in receptor tyrosine kinase signaling pathways in tumor protein p53 (TP53) [6], allelic loss of phosphatase and tensin homolog (PTEN) and epigenetic dysregulation, such as methylguanine methyltransferase (MGMT) promoter methylation [14], and loss of heterozygosity (LOH) 10q23 presentation [9] and high levels of CD44 [15] (Table 1). Here, PTEN is linked to glioblastoma.