In a mouse model of acute myeloid leukemia, expression of B7-H1 (also known as PD-L1, the ligand for PD-1) or B7-1 (also regarded as CD80, the ligand for CTLA-4) could contribute to the prolonged persistence of tumor cells via inhibiting CD8+ T cells-mediated killing (23), which pointed out another possible mechanism in which CD8+ T cells are involved in cancer dormancy. Here, CTLA4 is linked to neoplasm.