Given that EBV-infected B cells with type III latency constitutively express a variety of T cell-attracting chemokines, including RANTES [45] and IP10 [63], the ability of tumor endothelial cells to differentiate into HEV structures may act as a critical gate-keeper in controlling tumor T cell infiltration into EBV-induced lymphomas. The gene discussed is CXCL10; the disease is lymphoma.