The study suggests that the D262N mutant GFI1B feeds back on the function of the wild-type, unmutated GFI1B with the consequence that myeloid differentiation of precursors is favored over erythroid differentiation resulting in higher cell survival in MDS patient samples, which would attribute a direct oncogenic role to this GF11B mutant. Here, GFI1B is linked to myelodysplastic syndrome.