GBM is a very heterogenic disease, with several different biomolecular markers that predict treatment response: methylation status of the gene promoter for O6-methylguanine-DNA methyltransferase (MGMT) and isocitrate dehydrogenase enzyme 1/2 (IDH1/2) mutation are common in de novo GBM, and indicate a form of GBM more responsive to treatment (Thakkar et al., 2014[117]). This evidence concerns the gene MGMT and glioblastoma.