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. Here, MET is linked to hepatocellular carcinoma.