In AML cells harboring FLT3 internal tandem duplication (FLT3/ITD) mutation, a genetic aberration found in about 30 % of all AML patients, constitutively active Rac1, in concert with PAK1, was shown to bind directly to the signal transducer and activator of transcription 5 (STAT5), inducing STAT5 phosphorylation at Y694. Here, FLT3 is linked to acute myeloid leukemia.