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Early detection and interception of pancreatic ductal adenocarcinoma (PDAC) remain the only realistic strategies to reduce mortality and meaningfully extend survival.1 Among established precursors, cystic neoplasms—primarily intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms—offer a unique, although infrequent, window for secondary prevention. Retrospective analyses indicate that fewer than 10% of PDACs arise from cystic precursors.2 Yet, preventing even this proportion would constitute a major clinical breakthrough and could spare thousands of patients from a highly lethal malignancy.