RT can stimulate anti-tumor immune responses in several ways: (1) by enhancing major histocompatibility complex (MHC) class I surface expression, activating DCs, and promoting cross-presentation of tumor antigens that activate CD8+ T cells; (2) by increasing the release of chemokines and promoting margination and extravasation, which elevate the density of tumor-infiltrating lymphocytes; and (3) by upregulating FAS surface expression, leading to programmed cell death [23]. The gene discussed is CD8A; the disease is neoplasm.