Altogether, the de novo RRD glioblastomas had a distinct genomic landscape compared to the other 450 conventional IDH-wildtype glioblastomas, with a unique spectrum of oncogenic driver events that were predominantly short somatic mutations (single nucleotide substitutions or small insertions/deletions) targeting TP53, PTEN, NF1, ATRX, SETD2, and PDGFRA, along with a paucity of focal amplification and gene deletion events that are frequent in conventional IDH-wildtype glioblastoma (e.g., EGFR amplification, CDKN2A/B homozygous deletion, CDK4 amplification, MDM2 and MDM4 amplification). This evidence concerns the gene TP53 and glioblastoma.