These results are in agreement with findings in a different retrovirally expressed MLL-AF9 mouse model (Hanoun et al., 2014) and contrast with findings in myeloproliferative neoplasms (Arranz et al., 2014; Drexler et al., 2019), suggesting that the same niche cells exhibit different alterations and roles in various myeloid malignancies. Here, KMT2A is linked to myeloproliferative disorder.