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Correspondingly, interferon response-inducible Mx1-Cre -mediated inhibition of KAT2A in a retroviral-delivered MLL-AF9 model of AML in mice led to the depletion of AML stem-like cells, imposing a mild delay to disease initiation and severely impairing AML propagation, accompanied by a specific loss of H3K9 acetylation at a subset of promoters [83]

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