Researchers from The Jackson Laboratory (JAX) reported an epigenetic strategy that reactivates the tumor suppressor ZBTB7A in acute myeloid leukemia (AML) models. In a mouse study published in Science Translational Medicine, the team used a combined FISHnCRISP approach with CRISPR-based editing to identify ZBTB7A as epigenetically silenced in AML. They then showed that blocking KDM4 enzymes restored ZBTB7A expression and reduced leukemia burden while largely leaving normal blood formation unaffected. The result supports KDM4 inhibition as a potential non-chemotherapy route for AML biology—at least preclinically—and highlights an assay framework that could be applied to other silenced tumor suppressors.