Acute myeloid leukemias (AMLs) are characterized by chromosomal translocations involving the Mixed Lineage Leukemia (MLL) gene, which results in a variety of fusion oncogenes [1] derived from genes that are normally required during hematopoietic development; once fused, they induce epigenetic and transcription factor dysregulation [2]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.