CHOP is another primary target of induction of cell death after stress activation of ER.[27] It can be activated transcriptionally through all three branches of UPR: IRE1α, PERK/ATF4, and ATF6.[36] Treatment of pancreatic cancer cells with IRE1α inhibitors still caused induction of CHOP, suggesting CHOP was activated through ATF4 and ATF6. This evidence concerns the gene ERN1 and familial pancreatic carcinoma.