As EBNA1 is a viral transactivator expressed in all latently EBV-infected tumor cells and utilizes the OriP promotor for its activity, several studies have utilized an OriP-based vector to direct the expression of cellular toxins, such as driving cytosine deaminase expression (which converts the prodrug 5-flurocytosine to cytotoxic 5-flurouracil), or the herpes simplex virus TK, to make the cells susceptible to nucleoside analog antiviral drugs [53, 54]. The gene discussed is TKT; the disease is neoplasm.