This did not seem to be caused by a lesser proliferation rate of Flt3−/−MLL-ENL blasts as it was not accompanied by reduced leukemia infiltration of organs or longer disease latency, and the proliferation potential of the Flt3−/− and Flt3+/+MLL-ENL blasts was comparable upon ex vivo culture (Figures 3B and 4B). The gene discussed is KMT2A; the disease is leukemia.