TP53 and glioblastoma: Additionally, primary GBM-associated epidermal growth factor receptor (EGFR) amplification and phosphatase and tensin homolog (PTEN) loss deleted on chromosome ten, secondary GBM-associated tumor protein p53 (TP53) inactivation, PTEN loss, and telomerase reverse transcriptase (TERT) mutations, are all involved in the control of NSCs.99, 100, 101, 102, 103 Lee et al found that astrocyte-like NSCs with driver mutations spread from the SVZ, leading to GBM development in distal brain regions, providing direct genetic evidence for the theory that NSCs are the origin cells for GBM.104