In CML CD34+ cells, EZH2 inhibition plus TKI upregulated a number of BCL6 targets such as p53, despite BCL6 upregulation, suggesting that BCL6 and EZH2 share a number of targets, and that BCL6 mediated repression may be dependent on EZH2-PRC2 (Hurtz et al., 2011; Beguelin et al., 2016; Scott et al., 2016). This evidence concerns the gene TP53 and chronic myelogenous leukemia, BCR-ABL1 positive.