Combined with our findings that the absence of Rig-I in CD8+ T cells slows tumor progression in different settings of mouse models through facilitating the interaction of HSP90 and STAT5, the activation or upregulation of RIG-I in tumor-infiltrating T cells may represent a previously unappreciated obstacle that might counteract the antitumor effects initiated from RIG-I agonists within tumor or stromal cells. Here, CD8A is linked to neoplasm.