Our results showed that EMCV infection and 2C- or 3D-protein expression could phosphorylate the associated molecules of the PERK pathway and cleave the intact form of ATF6a (90 kDa), but they could not splice XBP1 mRNA, indicating that the activation of the PERK pathway and the ATF6a pathway can transiently block mostly protein translation and regulate the transcription of the ER chaperon against ER malfunction. Here, ATF6 is linked to infection.