Prolonged ER stress can result in apoptosis via ASK1 binding to IRE1, JNK activation, and phosphorylation of Bcl2 or CHOP mediated downregulation of Bcl2 levels[19] It therefore it seems plausible that EBNA3C is anti-apoptotic under conditions of prolonged ER stress such as might occur during initial EBV infection of resting B lymphocytes. Here, ERN1 is linked to Epstein-Barr virus infection.