In the present research, by a process of elimination, we determined that the downregulation of cFAM210A after HBx overexpression was attributed to m6A-dependent degradation via the YTHDF2-HRSP12-RNase P/MRP pathway and that cFAM210A inhibited tumorigenesis in HCC by suppressing the transactivation function of YBX1 toward MET but not by other mechanisms. This evidence concerns the gene YTHDF2 and hepatocellular carcinoma.