Functionally, the decreased drug sensitivity of MIXL1 expressing U937 clones shown in Fig. 1A is suggestive of an antiapoptotic advantage conferred through c-REL. Whereas this is the only readily detectable difference in U937 cells, in KG1 cells genetic ablation of endogenous MIXL1 results in loss of viability (Fig. 3D) which is rescued by c-REL. Such a significant difference between the two AML cell lines could be explained in part by the fundamental difference in the driver mutations in these cell lines. This evidence concerns the gene REL and acute myeloid leukemia.