Likewise, NUP98 fusion oncoproteins and the recently described UBTF (Upstream binding transcription factor) tandem duplications depend on the Menin–MLL1 complex to maintain a HOX/MEIS-centered gene expression programme; pharmacologic Menin–MLL1 blockade in NUP98-rearranged or UBTF-mutated AML displaces MLL1 and either the fusion or UBTF from target chromatin, downregulating HOXA/MEIS1 and inducing myeloid differentiation [56,57]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.