In cancer, ER stress promotes cancer development by triggering the UPR signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activating transcription factor (ATF) 6 [7,9,10], whereas prolonged and excessive ER stress can induce apoptosis through the inositol-requiring enzyme-1α (IRE1α)-mediated signaling pathway [11,12]. This evidence concerns the gene EIF2AK3 and cancer.