CCA pathogenesis is driven by chronic inflammation and cholestasis, which induce genetic and epigenetic alterations through persistent cytokine exposure, activate pro-survival (ERK1/2, Akt, and NF-κB) and pro-angiogenic (TGF-β, VEGF, and HGF) pathways, and promote EMT, metabolic reprogramming (c-Met, GLUT-1, and NIS), and stromal remodeling to enable invasion and metastasis [13]. This evidence concerns the gene HGF and cholangiocarcinoma.