While the sgScr-sgCas9; AML1-ETO recipients developed AML with an average latency of 64 days, both sgSsty1-sgCas9; AML1-ETO and sgSsty2-sgCas9; AML1-ETO mice developed AML with significantly shorter latency (56 days and 56 days, respectively) (Figure 2D). This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.