KMT2A and acute myeloid leukemia: A dominant negative mechanism also explains the puzzling result of why an MLL1 N terminus fused to the transcriptionally inert LacZ protein produces acute myeloid leukemia when knocked into the MLL1 locus in mice (101), and is consistent with studies showing specific sequences from the MLL1-N terminus and/or the fusion protein are required for cellular transformation (102, 103, 104, 105, 106).