An early knock-in model [30] utilized homologous recombination (HR) to generate an Mll-Af9 fusion gene and displayed a myeloproliferative disorder (MPD), leading primarily to AML characterized by expansion of immature myeloid populations with a small percentage developing B-cell ALL (B-ALL) [31]; thus, this model resembles the phenotypic heterogeneity of MLLr leukaemias, which can manifest as AML; ALL; or in a minority of cases, mixed phenotype acute leukaemia (MPAL). This evidence concerns the gene MLLT3 and acute lymphoblastic leukemia.