Experiments depleting RUNX1-ETO in established AML cells have shown that it is required to maintain leukemic growth (Ptasinska et al., 2012) but have also demonstrated that RUNX1-ETO-regulated gene expression is complex, with multiple genes being up- and downregulated after knockdown (Ptasinska et al., 2014, Ptasinska et al., 2019), indicating that the entire transcriptional network of such cells is rewired in the presence of the fusion protein. The gene discussed is RUNX1; the disease is acute myeloid leukemia.