Novel disease targets are necessary so as to improve acute myeloid leukemia (AML) patient outcomes, and epigenetic pathways are a focus.[1-3] We identified an oncogenic (Flt3ITD) pathway to epigenetic repression for the tumor suppressor DAPK1, by interaction of p52NF-κB and histone deacetylases (HDACs) on the promoter.[4] Suboptimal efficacy of single Flt3-selective tyrosine kinase inhibitors (TKI) is thought to involve such epigenetic collaboration.[4-6]. This evidence concerns the gene FLT3 and acute myeloid leukemia.