Given that Necdin null leukemia cells expressing either MLL-AF9 or AML1-ETO9a show enhanced apoptosis at 48 hours after AraC treatment (Figures 3E and 6E), it is likely that other mechanisms, including senescence, cell cycle arrest, and autophagy, may contribute to the differential response of leukemia cells expressing MLL-AF9 or AML1-ETO9a to AraC treatment. This evidence concerns the gene KMT2A and leukemia.