Unlike type II inhibitors, type I inhibitors reduce FLT3 phosphorylation in FLT3-ITD- and FLT3-TKD-mutated AML cells, while type II inhibitors can target FLT3-ITD but lack efficacy against TKD mutations, which exhibit secondary mechanism resistance to type II inhibitors1–3. This evidence concerns the gene FLT3 and acute myeloid leukemia.