Precursor lesions can be categorized as low, moderate, or high-grade dysplasia (carcinoma in situ), or alternatively they may exhibit invasive carcinoma.1,2 Among patients with resected IPMNs, 40–60% have developed to invasive carcinoma, and these patients have 5-year postresection survival rates between 30% and 55%.3,4 Tumor markers typically used to diagnose pancreas cancer, such as cancer carbohydrate antigen (CA) 19–9 and carcinoembryonic antigen (CEA), are not uniformly elevated in IPMNs. This evidence concerns the gene CEACAM5 and pancreatic neoplasm.