The superior anti‐tumor efficacy of anti‐RANKL/PD‐1 BsAb compared with the combination of anti‐RANKL plus anti‐PD‐1 antibodies may be explained by an enriched biodistribution of the BsAb to elevated levels of RANKL and PD‐1 expressed in the TME, including, but not limited to, co‐expression of both target antigens on CD8+ TILs. This evidence concerns the gene TNFSF11 and neoplasm.