Addition of anti-RL did not improve the response to anti-CTLA4 (or anti-PD-L1) in RANK−/− tumors as did in RANK+/+ tumors, suggesting that the augmented benefit of the anti-RL/anti-CTLA4 combination was driven by inhibition of RANK signaling in tumor cells (Fig. 4d). The gene discussed is TNFRSF11A; the disease is neoplasm.