While all models generated tumours, only the Nestin + H3.3K27M progenitors notably reduced tumour latency, while in the Olig2 + progenitors no differences were observed between H3WT and H3.3K27M tumours, owing to the conclusion that Nestin + cells (NSCs) are more vulnerable to H3K27M-driven postnatal transformation [74]. The gene discussed is NES; the disease is neoplasm.