In both MLL-AF9 and Meis1a/Hoxa9 leukemic models, recipients of Zeb1-KO LSCs succumbed to AML with enhanced rapidity compared with recipients receiving control LSCs, indicating that Zeb1 deletion accelerates LSC-mediated disease progression (Figure 8, F and G). The gene discussed is KMT2A; the disease is acute myeloid leukemia.