Correspondingly,interferon response-inducible Mx1-Cre-mediated inhibitionof KAT2A in a retroviral-delivered MLL-AF9 model of AML in mice led to thedepletion of AML stem-like cells, imposing a mild delay to diseaseinitiation and severely impairing AML propagation, accompanied by a specificloss of H3K9 acetylation at a subset of promoters[83]. This evidence concerns the gene KMT2A and acute myeloid leukemia.