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. The gene discussed is CEACAM5; the disease is neoplasm.