The JAK‐STAT pathway, activated by cytokines,[29] has been implicated in carcinogenesis and development in multiple tumors[30, 31] and is also able to regulate bile duct cell proliferation and function.[32] Similarly, PI3K‐AKT is a prominent signal transduction pathway activated in both solid and hematologic tumors.[33] In CCA, this pathway is known to play a central role in proliferation, cell cycle regulation, and metabolism.[34] We therefore assumed that CXCL6 may exert its effects in CCA through JAK‐STAT and PI3K‐AKT signaling. Here, SOAT1 is linked to cholangiocarcinoma.