Especially pertinent to this possibility are the findings of Wang and colleagues, who showed that lin-, bone marrow-derived progenitors subjected to retrovirus-enforced co-expression of Hoxa9 and Meis1 were more impaired with respect to B-lymphopoiesis and more potent in initiating acute myeloid leukemia than were cells transduced with Hoxa9 alone, suggesting that Hoxa9 and Meis1 may cooperate to mediate the hematopoietic effects of E2A-PBX1 that we observed in our experiments [53]. The gene discussed is PBX1; the disease is acute myeloid leukemia.