The Epstein–Barr virus (EBV) is a human gammaherpesvirus that can readily immortalize B lymphocytes in vitro, called lymphoblastoid cell lines (LCL). This immortalizing capability is relevant to understanding how EBV acts as the etiological agent of infectious mononucleosis and of often-fatal lymphoproliferative disorders in immunocompromised hosts [1]. EBV is also causally associated with endemic Burkitt lymphoma (BL) and undifferentiated nasopharyngeal carcinoma [1]. Over the past 15 years the array of human cancers potentially related to EBV has increased and now includes Hodgkin disease, subgroups of T or natural killer (NK) cell lymphoma, and gastric carcinoma [1–6]. These EBV-associated malignant diseases are clinically aggressive and often less responsive to conventional therapy, and currently available anti-herpesvirus (lyticcycle) drugs are ineffective treatments. A unique in vivo feature of EBV-associated malignancies is consistent existence (generally monoclonal) and expression of EBV exclusively in tumor cells and not in surrounding normal cells. In addition, considerable evidence has shown that EBV itself and some of its virus-encoded latent genes are actually implicated in certain critical aspects of the oncogenic event in cells