Here, using these cell lines and primary mutant CBL‐positive patient cells, as well as murine xenografts, we performed a side‐by‐side comparison of highly targeted and broad‐spectrum FLT3 inhibitors in late‐stage clinical development or FDA approved for mutant FLT3‐positive AML and demonstrated their ability to suppress mutant CBL‐positive AML proliferation and viability. Here, FLT3 is linked to acute myeloid leukemia.