While specific molecular dependencies have been identified for some genetic subtypes of AML, such as DOT1L or Menin inhibition for MLL-rearranged leukemias (Krivtsov et al., 2019), and CARM1 inhibition for AML1-rearranged leukemias (Greenblatt et al., 2019), distinct pathogenetic mechanisms of diverse AML subtypes also appear to converge on shared molecular pathways. Here, RUNX1 is linked to acute myeloid leukemia.