More specifically, genetic deletion of Hif-1α before leukemia initiation by different AML oncogenic mutations (AML1-ETO, MLL-AF9, HOXA9/MEIS1) revealed that loss of Hif-1α expression did not delay leukemia initiation or progression in any of the genetic models tested, and, contrary to previous data, its deletion either did not regulate or rather increased leukemia self-renewal in secondary transplantation experiments [26]. The gene discussed is HIF1A; the disease is acute myeloid leukemia.