Biologically, GBM radioresistance is driven by genetic heterogeneity, including EGFR amplification (57% per TCGA), phosphatase and tensin homolog (PTEN) mutations (40% per TCGA), cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) deletions (60% per TCGA), TERT promoter mutations (>70% per TCGA), and tumor stem cells [36,39]. This evidence concerns the gene CDKN2A and neoplasm.