In apparent contrast with these results however, recent evidence obtained in mouse models of AML suggests that genetic deletion of Hif-1α or Hif-2α may rather promote development and/or maintenance of LICs in the presence of specific leukemogenic mutations, such as MLL rearrangements or AML1-ETO, while having no apparent effect on the progression of established leukemia [26–27]. Here, KMT2A is linked to acute myeloid leukemia.