More importantly, METTL3 expression was not associated with HBV or HCV viral infection, suggesting that METTL3 upregulation may be a universal feature in the development of HCC with different etiologies [74] Overexpression of METTL3 can promote the proliferation and migration of HCC mainly because METTL3 can regulate the m6A modification of SOCS2 mRNA, it promotes the occurrence and development of liver cancer by reducing the stability of SOCS2 mRNA through m6A-YTHDF2-dependent pathways [75,76]. Here, SOCS2 is linked to viral infectious disease.