Potential and relevant mechanisms of action of anti-PD-1 antibody in the CNS have been summarized previously, including partial direct drug access to the tumor microenvironment, reinvigoration of local T lymphocytes in brain metastases, looser BBB due to production of IFNγ by reinvigorated T lymphocytes, and increases in circulating tumor-specific lymphocytes and antigen repertoire at least partially due to CNS antigen presentation in the peripheral lymph nodes through lymphatic vessels in the dura mater [95]. Here, IFNG is linked to neoplasm.