For this to occur, evolution to latent EBV infection is facilitated by the presence in premalignant epithelial cells of somatic mutations and alterations in cellular signalling, which activate telomerase and inactivate the tumour suppression genes RASSF1A and p16. Type II latent EBV infection occurs in undifferentiated nonkeratinizing carcinomas, in which the expression of the EBNA1, LMP1, LMP2A, EBERs and BART gene products facilitates the clonal expansion of infected epithelial cells [40]. The gene discussed is CDKN2A; the disease is neoplasm.