In line with this finding, tumour cells derived from relapsed FLT3/ITD‐mutated AML patients appear to be addicted to signalling from the constitutively activated FLT3 receptor tyrosine kinase which insinuates that less specific inhibitors may be efficacious earlier in therapy, while more specific inhibitors may be best utilized at relapse 29. This evidence concerns the gene FLT3 and neoplasm.