Furthermore, when we defined the antiproliferative effect as > 20% inhibition compared to untreated controls, we could not find any associations between those samples showing antiproliferative effects (higher versus lower than 20% inhibition by metabolic inhibitors) and AML cell differentiation (FAB classification, CD34 expression), cytogenetics, FLT3 or NPM1 mutations or occurrence of previous disease (versus de novo AML). This evidence concerns the gene FLT3 and acute myeloid leukemia.