A prior report suggested that A3A expression, but not activity, influenced survival and metastatic spread of pancreatic cancer (47); thus, we generated OVCAR3 and OVCAR4 cells with catalytically inactive A3A transgenes (A3A-C016S) and subjected them to the same treatment schema as in Figure 2A to enable assessment of deaminase activity. This evidence concerns the gene APOBEC3A and pancreatic neoplasm.