These results differ markedly from those obtained for lymphomagenesis in Eμ-myc mice, where disease was accelerated by loss of Bim, Puma or Bmf, although not Noxa.47, 48, 49 Thus, in contrast to Myc-driven lymphomagenesis, none of the BH3-only proteins tested appear to serve as a critical tumor suppressor for the development of MLL-driven AML. The gene discussed is BCL2L11; the disease is neoplasm.