Upon the depletion of Siah2, it increased the protein stability of PD-L1 and then inhibited T cells expansion and T-cell–mediated anti-tumor activity in CCA cells, indicating the clinical potential of the METTL14-Siah2-PD-L1–regulating axis for CCA immunotherapy (139). This evidence concerns the gene METTL14 and cholangiocarcinoma.