Engler et al. using immunohistochemistry demonstrated that there was an increase in the expression of eIF2α and CHOP proteins in human FECD tissues compared to non-diseased corneal tissues, indicating activation of the PERK-eIF2-ATF4-CHOP pathway of UPR/ER stress in FECD [17]. This evidence concerns the gene DDIT3 and Fuchs endothelial corneal dystrophy.