Expression of ASXL1-MT, but not ASXL1-MT-K351R, accelerated the development of AML induced by RUNX1-ETO9a, suggesting an oncogenic role for the monoubiquitinated ASXL1 mutant (Fig. 5b and Supplementary Fig. 5c–e). Here, RUNX1 is linked to acute myeloid leukemia.