In experiments using RCAS-TVA retroviral delivery, neonatal targeting of Nestin-positive brainstem progenitors with H3.3K27M accelerated tumours driven by Pdgfb overexpression and Trp53 loss18 Similarly, H3.3K27M decreased the latency of glioma formation in in utero electroporation experiments introducing H3.3K27M alongside Trp53 loss, Pdgfb overexpression, or WT or constitutively active (D842V) Pdgfra overexpression19,20. The gene discussed is TP53; the disease is neoplasm.