Researchers at St. Jude and Dana-Farber have identified key histone acetyltransferases—MOZ/KAT6A and HBO1/KAT7—that form critical complexes with NUP98 fusion proteins driving aggressive pediatric acute myeloid leukemia. This discovery reveals new molecular vulnerabilities that could be therapeutically exploited to disrupt malignant gene activation. Detailed proteomic mapping and functional validations herald a promising avenue for targeted therapies in refractory childhood leukemia subtypes.