Consistent with the significant proliferation inhibition of FLT3-ITD harboring cells, the phosphorylation of downstream effectors in the FLT3 signaling pathways, such as p-Stat5, p-AKT and p-ERK1/2 was also significantly inhibited by GNF-7 in AML patients harboring FLT3-ITD mutation, FLT3-ITD-dependent AML cells, and Ba/F3 FLT3-ITD cells, respectively (Fig. 1C, D, F). Here, AKT1 is linked to acute myeloid leukemia.