EZH2 inhibition: Highlighting the nuanced regulation of H3K27me3 in these tumors, residual PRC2 methyltransferase activity remains required for effective tumor growth, as genetic EZH2 loss impaired H3.3K27M-engineered mouse NPC xenograft growth and EZH2 inhibition with two different compounds (GSK343, EPZ6438/tazemetostat) led to growth arrest in human pHGG cells [27,59], though there have been conflicting reports regarding this in vitro finding [22,62]. This evidence concerns the gene EZH2 and neoplasm.