AML is a hematopoietic malignancy that is characterized by abnormal myeloid progenitor cell growth and a partial block in cell differentiation.1 There are several commonly detected mutations that confer a growth advantage to leukaemic cells, such as mutations in receptor tyrosine kinases (RTKs) (FLT3 and KIT, for example), non‐receptor tyrosine kinases (non‐RTKs) (JAK2 and ABL) and downstream signalling molecules such as RAS. Here, FLT3 is linked to acute myeloid leukemia.