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. The gene discussed is KMT2A; the disease is acute myeloid leukemia.