The genetic drivers of high-grade glioma (HGG) have been well-described, with isocitrate dehydrogenase (IDH) mutations and epidermal growth-factor receptor (EGFR) amplifications common in adult diffuse glioma, while pediatric HGG (pHGG) harbor high-frequency mutations in histones H3.1 and H3.3 as well as platelet-derived growth-factor receptor alpha (PDGFRA) alterations1–8. This evidence concerns the gene EGFR and malignant glioma.