AML with an internal tandem duplication of the FLT3 receptor (FLT3-ITD+ AML), which converts a ligand-responsive receptor into a constitutively active molecule, is a highly aggressive AML subtype that is frequently refractory to first line therapy.3 The FLT3-ITD mutation occurs on the background of other mutations, mostly in epigenetic regulators such as DNMT3 or TET2, or as a result of clonal evolution.4,5 For reasons that are as yet unknown, this mutation often occurs together with a mutation in nucleophosmin (NPM1). This evidence concerns the gene FLT3 and acute myeloid leukemia.