Signaling through CD137 induces the activation of CD8 + T cells in a CD28-independent manner, enhancing CD8 + T-cell survival, promoting their effector function in cancer and favoring memory CD8 + T-cell differentiation [48, 50], so the increase in these subsets may indicate that compared with patients with a poor response to treatment, in patients with a better response to treatment, CD8 + T cells can be significantly activated after treatment in terms of both quantity and ability and thus can effectively mediate the tumor-specific immune response. This evidence concerns the gene TNFRSF9 and cancer.