Hence, co-targeting FLT3 and CDK9 provides a rational therapeutic approach for the following reasons: (i) the activity of both kinases is required for the induction and maintenance of acute leukemia [25,27], and (ii) the upregulated expression of MCL-1 (which is dependent on CDK9) is one of the mechanisms for the development of resistance to FLT3 inhibitors [7]. This evidence concerns the gene FLT3 and acute leukemia.