Epstein–Barr virus (EBV) was the first virus shown to cause cancer in humans and is associated with a wide range of human cancers originating from epithelial cells, lymphocytes and mesenchymal cells. EBV-associated neoplasms affect both immune-competent hosts and immune-compromized patients who have received an organ transplant or who exhibit iatrogenic immune suppression. The development of an EBV-associated neoplasm is largely dependent on environmental factors and genetic susceptibility to viral infection that is associated with genetically prone immune deregulation.1