For example, ER stress can promote acinar cell apoptosis by activating the p53/AIFM2 axis and the PERK–JNK pathway,252–254,264 induce caspase-1-dependent pyroptosis via activation of the PERK pathway,265 and trigger necroptosis in pancreatic acinar cells by enhancing CTSB maturation and activating the PKCα–JNK–c-Jun cascade.266 On the basis of the above mechanism, targeting ER stress–related pathways to modulate acinar cell death may represent a promising therapeutic strategy for improving the pathological progression of AP. This evidence concerns the gene CTSB and alkaline phosphatase measurement.