Indeed, genes that are typically mutated in GBM, such as phosphatase and TENsin homolog deleted on chromosome 10 (PTEN), epidermal growth factor receptor (EGFR), isocitrate dehydrogenase (IDH1), p53, and v-raf murine sarcoma viral oncogene homolog B1 (BRAF), drive downstream metabolic pathways divergent from those found in healthy cells and are strictly dependent on the TME. This evidence concerns the gene TP53 and glioblastoma.