FMS like tyrosine kinase 3 (FLT3; CD135) is associated with poor clinical outcome in AML as it promotes cell proliferation and survival through the activation of the PI3K, RAS, and STAT3 signaling pathways (Stirewalt and Radich, 2003), and is reportedly mutated in approximately 30% of AML patients (Figure 2; Daver et al., 2019). This evidence concerns the gene STAT3 and acute myeloid leukemia.