EZH2 and leukemia: Neff et al. (2012) investigate this phenomenon and find that EZH2 loss weakens but does not completely eliminate leukemia growth. Genome-wide analysis of PRC2-mediated histone H3 trimethylation shows that H3K27me3 persists at specific loci despite EZH2 inactivation, indicating partial compensation by EZH1, as seen in embryonic stem (ES) cells (Shen et al., 2008).