Our research team has discovered dual-target inhibitors for the treatment of acute myeloid leukemia (AML) by targeting oncogenic kinase (FLT3) and epigenetic signaling (TAF1) with a single compound to overcome resistance mechanisms. At low concentrations, these novel drug-like compounds efficiently inhibit the growth of AML cell lines, and show low general toxicity in innovative pluripotent stem cell assays. FLT3 mutations are the most common mutations in AML, and our compounds have the potential to produce significant value to those AML patients developing resistance to FLT3-targeted therapies.