Forced overexpression of PBX3 along with its cofactor MEIS can transform normal hematopoietic stem cells in mice, leading to the formation of AML with a latency period similar to that observed for MLL-AF9, the most commonly observed oncogenic gene fusion, and a corresponding upregulation of HOXA cluster genes [36]. The gene discussed is PBX3; the disease is acute myeloid leukemia.