ZNF217 and precursor B-cell acute lymphoblastic leukemia: Specifically, ZNF217 depletion in B-ALL cells caused a more pronounced increase in H3K27ac levels than in H3K4me1 and H3K4me2 levels (Figure 4I-4J), suggesting that the regulation of H3K27ac may be more central to ZNF217's oncogenic role than does the regulation of H3K4me1 and H3K4me2.