RAE1 and cancer: IR stimulates immunity through IFN-mediated induction of MHC class I on cancer cells (15), activates DCs through IFN signaling (3, 4, 16, 17), releases DAMPs (3, 4), increases the T cell repertoire (18–20), attracts effector T cells by induction of CXCL16 in cancer cells (21), and helps maintain stable interactions between tumor cells and T cells by upregulation of RAE-1 (22) — all stimulatory for antitumor immunity.