As we know, in the tumor microenvironment, the expression of PD-1 on the surface of tumor cells and the combination of PD-L1 on the surface of tumor-infiltrating lymphocytes can inhibit the activity of T cells, lead to the loss of function of effector factors TNF-a, IFN-gamma, and IL-2, and inhibit cytolysis function through granulozyme B and perforin, and ultimately promote immune escape (12, 13). Here, PRF1 is linked to neoplasm.