A 40-year-old woman presented to the outpatient department of our hospital with a 2-year history of abdominal pain, which had worsened in the past few days. There were no other constitutional symptoms; in particular, there was no weight loss or loss of appetite. The serum amylase and serum lipase levels were always within normal limits, even during the current episode. There was no history of pancreatitis, alcohol abuse, drug use, or trauma. The patient was evaluated at an outside clinic 2 years ago and underwent imaging, including US and dedicated pancreatic CT , which revealed a complex multiseptated noncalcified pancreatic cystic lesion. After CT , the patient underwent endoscopic US, which showed the lesion was suspected to be an infected parasitic cyst; fine-needle aspiration and cytology were not attempted due to the risk of iatrogenic rupture. The patient was advised to undergo surgical resection but declined the procedure and was lost to follow-up for 2 years before her current visit to our facility. On clinical examination, there were no clinically important findings, aside from mild to moderate pain on deep palpation and some shifting dullness that was suggestive of ascites. The patient always remained hemodynamically stable. US-guided ascitic fluid analysis was performed, which revealed amylase levels of 869 IU/L (normal range, 4–234 IU/L). Considering prior CT and endoscopic US reports, the patient was further evaluated with a pancreatic MRI protocol for lesion characterization and to explain the new-onset abdominal pain (Figs 1, 2).Axial T2-weighted images at the level of the pancreatic body revealed a thick-walled (.2 mm) multilocular hyperintense cystic lesion with free fluid in perihepatic and perisplenic locations (Fig 1A). Discontinuity of the wall of the cystic lesion was noted in the anteroinferior aspect, with rupture of the contents into the mesocolon (Fig 1B). Coronal T2-weighted imaging (Fig 1C) revealed similar findings, with rupture along the inferior aspect and spillage of contents in the mesocolon. A coronal T2-weighted thin-slab maximum intensity projection image (Fig 1D) revealed the rupture and showed the main pancreatic duct, with no obvious communication with the lesion. Unenhanced T1-weighted MRI scan (Fig 2A) showed hyperintense septae and wall (Fig 2B). Contrast-enhanced T1-weighted nonsubtracted image showed wall and septal enhancement within the lesion, which was substantiated on subtraction images (Fig 2C, 2D). The septae appeared irregular and mildly nodular at places that were concerning for malignant transformation. The patient underwent distal pancreatectomy and splenectomy, with resection of the transverse mesocolon because of peritoneal spillage. Surgically, there was a defect in the inferior aspect of the lesion, with contents bulging into the mesocolon, and there was some extension intraoperatively into the inframesocolic compartment (Fig 3A, 3B). Pathology revealed the lesion was composed of multiple individual mucin-filled cysts that were inseparable from the resected pancreatic tissue. Microscopic examination of the cysts showed lining of tall columnar mucin-secreting epithelium having basally located nuclei and supranuclear vacuoles. Subepithelial stroma showed densely packed spindle-shaped cells simulating ovarian-type stromal hyperplasia, and there were areas of nuclear atypia and stratification suggestive of high-grade dysplasia (Fig 4A, 4B). No mitosis or invasion was detected to suggest frank malignancy. Immunohistochemistry expressed progesterone positivity, which enabled us to confirm the diagnosis (Fig 4C). What is your diagnosis?