Researchers at The Jackson Laboratory (JAX), working with collaborators, reported that inhibiting KDM4 can epigenetically reactivate the tumor suppressor ZBTB7A in acute myeloid leukemia (AML) models. The study, published in Science Translational Medicine, used FISHnCRISP—combining fluorescence in situ hybridization, flow cytometry, and CRISPR editing—to identify ZBTB7A as a silenced gene. In mouse AML data, blocking KDM4 restored ZBTB7A expression and reduced leukemia burden while largely preserving normal blood formation, according to the report. The results point to a targeted epigenetic approach that seeks to restore tumor-suppressive function rather than relying only on cytotoxic chemotherapy concepts.