More recently, Roychoudhury et al. [38] found that HLF overexpression could rescue colony forming deficits in the absence of Meis1 in MLL-fusion models of AML, supporting Hlf as a key downstream mediator of Meis1 function in both normal hematopoietic and leukemic processes. This evidence concerns the gene KMT2A and acute myeloid leukemia.