In addition, the finding that Nup98 fusions with different translocation partners can be recruited to HOX and Meis1 genes (Xu et al. 2016), along with our observation that the N-terminal portion of Nup98 can promote H3K4me3 and gene activation at aberrant sites, provides a unifying model for how Nup98 translocation proteins trigger AML (Fig. 6B). Here, MEIS1 is linked to acute myeloid leukemia.