Despite the low number of cells coexpressing KMT2A-MLLT3 and FLT3N676K, mice receiving cotransduced cells succumbed of leukemia much earlier than those receiving cells only transduced with KMT2A-MLLT3 (median latency 34 days vs 50 days for KMT2A-MLLT3 alone), confirming that subclonal activating mutations in FLT3 accelerate KMT2A-MLLT3 leukemogenesis Hyrenius-Wittsten.74 Disease latency in secondary recipients was just slightly different (median latency 16 days vs 21 days for KMT2A-MLLT3 alone). The gene discussed is MLLT3; the disease is leukemia.