Secondly, bile−acid (BA) metabolism and signalling represent another targetable vulnerability: dysregulated BA pools and receptor signalling (e.g., FXR, TGR5) alter immune and stromal−cell behaviour in the gut–liver/biliary axis of CCA, and modulation of BA receptors or transporters provides a metabolic “trap” to disrupt tumour–immune crosstalk (245). The gene discussed is GPBAR1; the disease is cholangiocarcinoma.