In MV4;11 cells, harboring FLT3-ITD mutation, ASC at high concentrations downregulated FLT3 phosphorylation and that of its p-Stat5a/b target proteins, indicating potential activity of the drug in the subset of FLT3-ITD positive AML, notoriously characterized by poor prognostic outcome. This evidence concerns the gene FLT3 and acute myeloid leukemia.