Furthermore, we show that CTLA-4/PD-1 blockade increases the ability of T cells from EBV-infected mice to produce interferon in response to EBV antigens in vitro, enhances T cell infiltration into EBV-induced lymphomas, and increases the number of tumor-associated high endothelial venules (a specialized endothelial cell type required for T cell migration into tumors) [41–43]. The gene discussed is CTLA4; the disease is neoplasm.