However, there are some reports on MLLr leukemia that develop lineage switch without clonal evolution, suggesting that factors other than genetic change can target lineage switch.8,25,49 Among them, epigenetics may play a role, given that the accessibility of genome chromatin and transcription factor binding sites in tumor cells change during lineage switch.50 MLL fusion protein is different between AML and ALL,45,51 as KMT2A-AFF1 translocation is almost only present at diagnosis as B-cell ALL, and the KMT2A fusion form plays an important role in determining the binding site of the oncogene. This evidence concerns the gene KMT2A and acute lymphoblastic leukemia.