This genomic instability lays the groundwork for cancer transformation and malignant glioblastoma behavior, which is characterized by evasion of senescence (telomerase or telomere length affecting mutations), escape from growth and invasion control (biallelic CDKN2A deletion), activation of growth factor signaling pathways (EGFR or PDGFR (platelet-derived growth factor receptor) gene amplification), and resistance to programmed cell death (TP53 mutation). This evidence concerns the gene TP53 and glioblastoma.