Since those factors also bind to other enhancers that recurrently translocate to EVI1 in t(2;3)(p21;q26), t(3;7)(q26;q24), t(3;6)(q26;q11), or inv(3)/t(3;3)(3q26;3q21) AML, we argue that EVI1 expression is driven by a common mechanism. The gene discussed is RUNX1; the disease is acute myeloid leukemia.