Indeed, the METTL3–METTL14depletion was shown to prevent the maturation of pri-mR126 to miR126,an oncosuppressor found in low amounts in patients with metastasesand relapsed forms of HCC.104 On the otherhand, METTL3-mediated methylation leads to the degradation of themRNA of suppressor of cytokine signaling 2 (SOCS2), an oncosuppressorwhose downregulation facilitates tumor growth and metastasis.105 Furthermore, METTL3 activity supports HCC metastatization,as m6A deposition is crucial for EMT. This evidence concerns the gene SOCS2 and hepatocellular carcinoma.