In adults, the key distinction is between IDH1 mutant (G-CIMP/ATRX/TP53 or 1p19q co-deleted/TERT promoter mutated) and WT (classical, mesenchymal, PA-like) (Ceccarelli et al., 2016), whereas in the childhood setting IDH1 mutations were restricted to a small proportion (6.25%) of tumors mostly in adolescents (representing the tail end of an overwhelmingly adult disease), and harbored only rare examples of the common alterations seen in WT adult GBM (e.g., 4.9% EGFR mutation/amplification). This evidence concerns the gene TP53 and glioblastoma.