For instance, HDACi Panobinostat treatment of a mouse model of AML bearing the AML1/ETO fusion triggered terminal myeloid differentiation with a remarkable anti-leukemic response19, and treatment with small-molecule inhibitors against IDH1/2 also induced myeloid differentiation in AML models with mutant IDH1/220,21. The gene discussed is RUNX1; the disease is acute myeloid leukemia.