About 30% of adult AML patients with a normal karyotype have an FLT3-ITD mutation, which is an internal tandem duplication of the FMS-like tyrosine kinase receptor gene.[70] AML with FLT3-ITD has a poor prognosis, a greater chance of relapsing, and consequently, a worse overall and disease-free survival.[71] To treat AML, it is crucial to specifically block FLT3 kinase activity, and multiple FLT3 inhibitors have been clinically produced. This evidence concerns the gene FLT3 and acute myeloid leukemia.