As expected the majority of differentially expressed genes were upregulated in the PDGF-B; H3.3K27M; p53-deficient model relative to the PDGF-B; p53-deficient tumor as the H3.3K27M mutation is thought to contribute to tumor formation through inhibition of the polycomb repressive complex 2 or PRC2, an H3K27 methylase complex that is associated with gene repression. This evidence concerns the gene TP53 and neoplasm.