Reports indicate that approximately 40% of cholangiocarcinoma cases harbor genetic alterations that can be targeted by specific therapies.[1] The prevalent molecular alterations include isocitrate dehydrogenase 1 mutations (15%–20%), fibroblast growth factor receptor 2 (FGFR2) fusions (10%), HER2 amplifications and mutations (5%–10%), and proto-oncogene BRAF mutations (3%).[2] Consequently, various drugs targeting different mutational profiles are being explored for the treatment of advanced cholangiocarcinoma. Here, BRAF is linked to cholangiocarcinoma.