Therefore, these suggest that in normal HSCs, HIF-1α and RUNX1 interaction is increases RUNX1 activity to induce angiogenesis or HSC differentiation, but in leukemic states, HIF-1α and RUNX1(AML)/ETO fusion protein interaction increase leukemic aggressiveness with proliferating phenotypes. The gene discussed is RUNX1; the disease is acute myeloid leukemia.