ZBTB16 and acute myeloid leukemia: Our observations in SS models are reminiscent of findings in the AML context showing that the chimeric proteins PLZF/RARa and AML-Eto mediated the reduction or loss of heparanase activity, likely as a consequence of impaired myeloid differentiation, and that treatment with the HDACi trichostatin A reversed the downregulation of heparanase expression induced by the AML-Eto [127].