Although other in vivo model should be used to address the role of SET in leukemogenesis, these results are consistent with published data in chronic myeloid leukemia [5, 54] and other human cancer cells [5, 7, 8, 37, 39, 55], and strongly suggest that SET deregulation may play an important role in the pathogenesis of leukemia in AML patients. The gene discussed is SET; the disease is leukemia.