The most frequent oncogenic driver events in the de novo RRD glioblastomas were inactivating mutations in the TP53 (8/9, 89%), PTEN (7/9, 78%), and NF1 (5/9, 56%) tumor suppressor genes, which are known to be important glioblastoma tumor suppressors but were present at lower frequency in both our conventional IDH-wildtype glioblastoma cohort (TP53: 130/450, 29%; PTEN: 254/450, 56%; NF1: 84/450, 19%) and other prior glioblastoma datasets such as The Cancer Genome Atlas [10]. This evidence concerns the gene PTEN and neoplasm.