Consistent with this finding, endogenous EBV replication is suppressed in type III NPC, rendering the virus latent.39 Thus, we speculate that elevated BST2 expression likely results from latent EBV infection in type III NPC, and that BST2 may have multiple functions in EBV latency, oncogenesis and cisplatin resisitance. This evidence concerns the gene BST2 and nasopharyngeal carcinoma.