A 75-year-old woman was hospitalised for management of obstructive jaundice and intermittent epigastric pain in August 2020. Contrast-enhanced computed tomography (CT) showed a mass at the head of the pancreas, encasing the superior mesenteric vein (). Positron emission tomography CT further delineated a mass in the uncinate process of the pancreas (size = 4.1 * 3.6 cm; SUV = 18.2) without a clear boundary with the duodenum. However, no distant metastases were detected. Endoscopic retrograde cholangiography revealed dilatation of the common bile duct, and an EBD tube was placed to drain the bile. The brush biopsy was unremarkable for malignancy. CT-guided fine needle aspiration biopsy of the pancreatic mass was concordant with adenocarcinoma, and the patient was diagnosed with potentially resectable PDC. The tumour marker, carbohydrate antigen 19-9 (CA19-9), was mildly elevated at 50.3 U/mL. After discussion, the multiple disciplinary teams recommended induction therapy followed by surgery, but she refused both surgery and radiation therapy and agreed only to chemotherapy. Chemotherapy was commenced with modified FOLFIRINOX (leucovorin/5-FU/irinotecan/oxaliplatin). The first cycle was uneventful, but the second cycle was complicated by hospital admission for the management of diarrhoea, dehydration and urosepsis. The patient refused any further intravenous chemotherapy. She was willing, however, to try other oral options. Comprehensive genomic profiling using liquid biopsy to perform next generation sequencing of the cell-free DNA (Guardant 360 CDX) was requested. The test detected KIT amplification at a plasma copy number of 2.2. The tumour was microsatellite stable. Given the patient’s willingness to attempt new treatments that could provide her relief and improve her quality of life, treatment with KIT inhibitor was discussed and agreed to start, which had never been attempted in this population of patients. Imatinib, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet derived growth factor receptors (PDGFRA), and c-KIT, was started on a 400-mg daily dosage []. Imatinib was chosen considering its ready availability and reasonable price as compared to other potential targeted therapeutics for c-KIT. In addition, it is a quite tolerable option. On a follow-up consultation a month after the start of treatment, the patient reported feeling well, her performance status improved to ECOG 0, and CA19-9 dropped to 7. Three months after commencing maintenance imatinib (5 months after her initial diagnosis), imaging revealed an excellent ongoing response with stable disease. However, biochemical progression was evident in rising CA19-9 up to 117, possibly representing a resistant clonal population. Because she refused intravenous therapy, capecitabine was added to the ongoing imatinib therapy, at a reduced dose of 1 g bid × 1 week alternating with 1 week break off therapy. An alternate week schedule was used to improve tolerability as the patient developed GII/III ‘Hand-Foot syndrome’. Since imatinib was well tolerated, we continued imatinib with capecitabine. Ongoing therapy with imatinib and capecitabine has been well tolerated, and she remains clinically well with excellent PS. CA19-9 dropped down to 11. Imaging at 16 months after the addition of capecitabine (20 months after her initial diagnosis) has revealed stable disease, with no metastatic disease on CT imaging (). The patient described in this report provided informed written consent for the collection and publication of her deidentified data – clinical, molecular and images – from her medical records.