EGFR and neoplasm: H3 G34-mutant tumors are probably initiated by the histone 3 mutation but additionally carry frequent genetic alterations in other genes including ATRX, TP53, PDGFRA, EGFR, CDKN2A, and others.3,4,8–13 Half of the tumors exhibit activating PDGFRA mutations or PDGFRA gene amplification that are selected for at tumor recurrence; furthermore, the H3 G34 mutation may no longer be required for tumor growth, whereas mutant PDGFRA may drive recurrence,28 suggesting that it may represent a druggable target for therapeutic intervention.