To strengthen our hypothesis of synergy between immune checkpoint therapy and Nr2f6 inhibition as intracellular immune checkpoint target, we next tested the αCTLA-4 treatment in wild-type and Nr2f6−/− mice injected with B16-OVA cells showing superior tumor rejection and strongly enhanced survival in the double treatment group (Fig. 3a-d). Here, NR2F6 is linked to neoplasm.