Given that transduction of the same MLL-mAf4 gene into human HSPCs and transplantation in immune-compromised mice induced pro-B ALL17, it appears that murine HSPCs tend to develop myeloid lineage leukemia through the MLL-AF4 fusion protein, whereas human HSPCs tend to develop lymphoid lineage leukemia. The gene discussed is KMT2A; the disease is leukemia.