Mutations in tumor suppressor genes, such as tumor protein 53 (TP53), PTEN, and neurofibromatosis type 1 (NF1), whose downstream altered pathways drive GBM development, are also closely related to peritumoral hyperexcitability, as observed in epileptogenic GBMs developed in a PTEN, NF1, and p53 CRISPR-based animal model [63,64,65]. The gene discussed is PTEN; the disease is glioblastoma.