Together, the commonalities discussed in this study might present novel entry points for further treatment of AML patients with these translocations, for example by targeting the RUNX1/ETS-factor interaction, disruption of the associated complex, or use of specific compounds that target one of the common pathways altered by the fusion proteins, such as BCL2 inhibitors [34, 35] to block the activation of the anti-apoptosis program. Here, RUNX1 is linked to acute myeloid leukemia.