Consistent with METTL16 mediated regulation of PRDM15-FGFR4, our data revealed that depletion of METTL16 by its GapmeR antisense oligonucleotide (ASO) decreased the protein levels of PRDM15 and FGFR4 in CCA cells (Fig. 6F). This evidence concerns the gene PRDM15 and cholangiocarcinoma.