As a hypothesis, this abnormal hyper-processing of the C-terminal end of the apoA2 homodimer was anticipated to be caused by the activity of circulating pancreatic enzymes due to minor pancreatitis with pancreatic cancer or other pancreatic disorders, and the abnormal hypo-processing pattern was presumed to occur by reducing the circulating pancreatic enzymes due to pancreatic atrophy and insufficiency. This evidence concerns the gene APOA2 and pancreatic neoplasm.