The differing stages of arrested B-lineage differentiation may be attributable to the different instructive capabilities of different KMT2A fusions, as suggested by a reported model system30, in which genetically concordant human CB HSPCs were transformed into pro-B and pre-B-ALL by KMT2A-Aff1 and KMT2A-MLLT3, respectively. The gene discussed is AFF1; the disease is acute lymphoblastic leukemia.