The increased mutational frequency of EGFR (a tyrosine kinase receptor), NF1 (a RasGAP) and PTEN (a phosphatidylinositol (3,4,5)-trisphosphate phosphatase) in tumor samples of patients with high PREX1 expression suggested that these oncogenic drivers, known to contribute to the classification of a subpopulation of LGG patients (52, 53), might regulate PREX1 expression. Here, EGFR is linked to neoplasm.