Improved understanding of the genetic and epigenetic landscape of AML has enabled the development of targeted therapies for recurrent oncogenic mutations, such as those affecting the cytokine transmembrane receptor Fms-like tyrosine kinase 3 (FLT3), present in 30% of cases, and isocitrate dehydrogenase (IDH1/2), present in 20% of cases [2–5]. This evidence concerns the gene FLT3 and acute myeloid leukemia.