ZIKV infection has been shown to promote XBP1 splicing and XBP1s translocation into the nucleus, leading to elevated expression of XBP1 downstream effectors such as ER degradation-enhancing α-mannosidase-like 1 (EDEM-1) and CHOP, indicating the activation of the IRE1 arm of the UPR [48]. This evidence concerns the gene XBP1 and Zika virus infectious disease.