Acute myeloid leukemia (AML) is a form of blood cancer, which originates in the bone marrow and features an expanded subset of white blood cells, called myeloid cells. The maturation of these myeloid cells requires genetic programming, which is ensured by specific proteins called transcription factors. We have observed that loss of the transcription factor Gfi1 leads to an accumulation of myeloid cells in mice that is reminiscent of a condition that often precedes overt myeloid leukemia. We have also discovered a variant of the Gfi1 gene in AML patients and we believe that carriers of this gene variant, who suffer from a specific AML subtype, have a much worse prognosis than non-carriers. We wish to determine the role of Gfi1 in AML and to validate the new Gfi1 gene variant as a prognostic marker for AML. The results of our studies will help to better identify persons who are at risk of developing AML and to make better therapeutic decisions for patients that suffer from this disease.