In vitro experiments have demonstrated that co-culturing cholangiocarcinoma (CCA) cells with CagA-positive Helicobacter species leads to higher expression levels of the antiapoptotic factor Bcl-2 and the activation of mitogen-activated protein kinase and nuclear factor-kappa B (NF-κB) signaling pathways, resulting in the further proliferation of bile duct cancer cells. Here, BCL2 is linked to cholangiocarcinoma.