For two AML sub-types, the t(8;21) translocation which expresses an aberrant RUNX1 fusion protein, RUNX1-ETO and the FLT3-ITD which expresses a constitutively active receptor for the cytokine FLT3-ligand, we were able to gain insights into the molecular mechanism of RUNX1 action, the signals activating AP-1 and its genomic targets involved in driving cell proliferation. Here, JUN is linked to acute myeloid leukemia.