MLLT3 and acute myeloid leukemia: Consistent with this, Hyrenius-Wittsten et al. [215] demonstrated that co-expression of KMT2A/MLLT3 and FLT3N676K in human CD34+ UCB HSPCs mainly resulted in the development of AML in NSG mice, concluding that constitutively active signaling mutations within the transduced cell could replace exogenous factors and promote AML.