Given the demonstrated effectiveness of FLT3 inhibitors against leukaemia characterized by mutated CBL and consequent increased expression of wt FLT3, we were interested in exploring this phenomenon more thoroughly across a panel of widely investigated FLT3 inhibitors in late‐stage clinical development or that have been FDA approved for mutant FLT3‐positive AML. This evidence concerns the gene FLT3 and acute myeloid leukemia.