Although β-secretases are known to cleave molecules in addition to APLP2 (50–52), and cleavage of other proteins may contribute to the effect of β-secretase inhibitors on pancreatic cancer cell viability, these results are consistent with the notion that APLP2 cleavage fragments influence the survival of pancreatic cancer cells, and they suggest that further investigation of the efficacy and mechanism of β-secretase inhibitors as potential therapies for pancreatic cancer is warranted. This evidence concerns the gene APLP2 and pancreatic neoplasm.