Figure 8. A summary of the findings.

A new epigenetic mechanism involved in the pathogenesis of CML-BP: by binding to promoter and demethylation of trimethylated H3K4 at the miR-21 locus, RBP2 downregulates miR-21 expression, which in turn activates PDCD4. In CML progression, low levels of RBP2 cannot repress the expression of miR-21, which decreases PDCD4 expression to block cell differentiation and stimulate cell proliferation.