AFF1 and leukemia: 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