By binding to C‐X‐C motif chemokine receptors (CXCRs), CXCLs activate several tumor‐associated pathways including MAPK, STAT, TGF‐β, and β‐catenin, thereby modulating the development and metabolism of tumor cells,[20, 21] hinting at a possible mechanistic link between chemokine signaling and CCA treatment resistance. Here, SOAT1 is linked to neoplasm.