This study systematically elucidates the central role of impaired autophagic flux in AP, untangles the causal relationship between lysosomal dysfunction (such as LAMP degradation and imbalance of cathepsin activity) and abnormal activation of pancreatic enzymes, and proposes that “autophagy activation with delayed flux” is a key feature of acinar cell injury in AP. The gene discussed is CTSS; the disease is alkaline phosphatase measurement.