Considering the overall tolerable profile and the tumor growth impact observed in vivo, we suggest de novo or relapsed AML patients with myelomonocytic/monocytic phenotypes and genetic aberrations associated with this maturation state (i.e., CBFB and KMT2A rearrangements, and Fms-related receptor tyrosine kinase 3 (FLT3) missense mutations) [1] as potential candidates for combinatorial ATP1A1 targeting strategies by CGs. The gene discussed is FLT3; the disease is acute myeloid leukemia.