To gain insight into the molecular drivers of GBM, studies have extensively profiled tumours, reporting both genetic and epigenetic mutations believed to play a part in tumour initiation and progression including loss of heterozygosity (LOH) 10q, amplification of epidermal growth factor receptor (EGFR), deletion of p16INK4a and mutations in tumour protein 53 (TP53) and phosphatase and tensin homolog (PTEN) (6). This evidence concerns the gene PTEN and glioblastoma.