In nasopharyngeal epithelial cells, infection with EBV at an early stage occurred simultaneously with slowing down the cellular growth and accelerating senescence, overexpression of cyclin D1 or its associated factors in the NPE cell lines, however, could counteract the EBV infection induced arrest and senescence (Tsang et al., 2012); this may be due to the activation of cyclin D1 pathway that enhances the aerobic glycolysis property and further overcomes the senescence, therefore enabling persistent infection of EBV and drives NPC pathogenesis. Here, CCND1 is linked to nasopharyngeal carcinoma.