Leukaemia initiation by KMT2A rearrangements is thought to occur via an improper expression and regulation of Hox genes.13 The KMT2A protein is a homologue of the trithorax protein in Drosophila melanogaster14 and functions as a transcriptional activator and regulator of Hox genes during embryogenesis and haematopoiesis.15, 16 AFF1 is a nuclear protein acting as transcriptional regulator involved in haematopoietic development of lymphoid precursors.17 The KMT2A‐AFF1 fusions are capable of initiating and maintaining an erroneous programme of transcription with oncogenic consequences.18 This evidence concerns the gene KMT2A and leukemia.