A 45-year-old woman was referred with a huge mass of the liver. She complained of a vague abdominal discomfort that had persisted for 1 month. She had no history of liver disease, and physical examination revealed mild abdominal distension. Pertinent laboratory test results were unremarkable. She had a history of small intestinal resection for a gastrointestinal stromal tumor (GIST) 11 years prior (Fig. 1A). Computed tomography (CT) showed a heterogeneous hypervascular tumor with central necrosis, occupying left hemiliver and right paramedian sector of the liver, measuring 20 × 13 cm (Fig. 1B). Positron emission tomography-CT using ¹⁸F-fluorodeoxyglucose showed intense hypermetabolic activity (maximum standardized uptake value 8.2) along the peripheral solid portion of the tumor with central photon defect area representing necrosis (Fig. 1C). A tumor biopsy revealed small round/spindle-shaped cells surrounded by fibrous tissue. Immunohistochemical stainings revealed vimentin reactivity, as well as CD117 reactivity. On c-kit sequencing, a deletion in exon 11 was identified. Based on the patient’s history, positive staining for CD117, and c-kit mutation results, the neoplasm was diagnosed as a metastatic GIST in the liver (Fig. 2). The pros and cons of using imatinib were discussed, and the patient was started at a dose of 400 mg/day and the dose had been tapered to 200 mg/day. One year follow-up CT showed the hepatic tumor slightly diminished in size, but stabilized at a size of 18 × 13 cm (Fig. 1D).

GISTs in the small bowel tend to be more aggressive than those in the stomach. The liver is most common metastatic site. Although hepatic metastasis of a GIST is not uncommon, delayed metastasis over 5 years later is extremely rare. A few cases of inoperable liver metastatic GISTs have been reported, most were treated by a multidisciplinary approach including imatinib administration and subsequent portal vein embolization leading to tumor shrinkage which enables curative resection.