Such fusion proteins, including ETV6-RUNX1 and TCF3-PBX1, and those involving PAX5, KMT2A (MLL) and tyrosine kinases such as BCR-ABL1, are typically acquired early in leukaemogenesis and drive tumour formation by perturbing cellular pathways including haematopoietic development, tumour suppression, kinase signalling and chromatin remodelling1, 2. The gene discussed is KMT2A; the disease is neoplasm.