The role of the GFI136N variant in the development of a myeloproliferative disorder that may lead to AML. Proposed model for the function of the GFI136N variant: diminished binding of GFI136N to the Hoxa9 locus as well as to other gene promoters results in epigenetic changes leading to deregulation of expression, in particular of the Hoxa9 gene and subsequently to a proliferative expansion of the GMPs. This effect of the GFI136N variant can increase the likelihood that an AML develops, if other cooperating events occur.