This intensivetreatment is only effective in a small subset of AML patients andthe therapeutic landscape has broadened in the last five years, drivenby the development of targeted therapies focused on genetic mutationspresent in the disease.46,47 NPM1 and fms-like tyrosinekinase 3 (FLT3) are the most frequent mutations in AML, with an incidenceof more than 50%,48 and therapies targetingspecific mutations appear to have great potential to improve prognosisand treatment. Here, NPM1 is linked to acute myeloid leukemia.