Our current study has some limitations: (i) since this study includes a single type of MLLr, MLL-AF9 fusion protein, to induce leukemia development in mice, it is unclear whether ASH1L has the similar function in promoting other MLLr-induced leukemogenesis; (ii) although Ash1L deletion induces cell death, some MLL-AF9-transformed cells survive in vitro and in vivo, suggesting the MLL-AF9-transformed cells have heterogenous responses to the Ash1L depletion. This evidence concerns the gene KMT2A and leukemia.