Both FLT3 and KMT2A::MLLT3 were viable targets to reduce growth of the AML cells after siRNA treatment under a variety of settings, and the combination of FLT3 and KMT2A::MLLT3 siRNAs enhanced the effect of delivering individual siRNAs, although full synergistic activity was not seen. This evidence concerns the gene FLT3 and acute myeloid leukemia.