AML is, thus, a highly aggressive disease, and although drugs that target different pathways (e.g., FLT3 tyrosine kinas, BCL-2 and IDH1/2) are now approved for the treatment of AML, with others being in different stages of development [9], overall survival rates are unfortunately still low, and show complications resulting from therapy and from the emergence of resistance [10]. The gene discussed is FLT3; the disease is acute myeloid leukemia.