From these experiments, we conclude that the endogenous truncation of the C’ terminal regulatory region of Ppm1d by CRISPR-Cas9 or ectopic expression of truncated PPM1D are similarly sufficient as expression of dominant-negative TP53 to potentiate the in vivo formation of brainstem gliomas in the setting of H3.3K27M and PdgfraD842V. The gene discussed is TP53; the disease is brain stem glioma.