Interestingly, distinct MLL fusion partners suggest a possible role in the tropism of the leukemia because certain partner proteins not only convert MLL to an oncogenic fusion protein but also direct the lineage susceptibility for transformation; MLL-AF4 expressing leukemias are mainly diagnosed as pro-B ALL in both pediatric and adult patients, whereas fusion partners AF9, AF6, or AF10 are common in myelomonocytic or monoblastic acute myeloid leukemia subtypes [9]. This evidence concerns the gene KMT2A and acute myeloid leukemia.