Myeloid leukemia (CML and AML) is particularly faced with the challenge of targeting cells that are treatment-resistant due to the large repertoire of mutations that arise, namely, point-mutations associated with BCR-ABL in CML or FLT3-TKD in AML (Corbin et al., 2011; Hamilton et al., 2012). The gene discussed is FLT3; the disease is acute myeloid leukemia.