Rearrangements involving KMT2A are often found in de novo and DNA topoisomerase II inhibitor therapy‐related myeloid and lymphoblastic acute leukaemias, with varying incidence according to type and age.1 Overall, KMT2A rearrangements account for 10% of all acute leukaemias2 but are predominantly found in infants between the age of 0 and 2 diagnosed with acute lymphoblastic leukaemia (ALL; 70%‐80% of cases3, 4) and in therapy‐related acute myeloid leukaemia (AML) patients (up to 70% of cases).5 Here, KMT2A is linked to acute myeloid leukemia.