In experiments investigating the underlying mechanism, we found that the expression levels of p-AKT, p-mTOR, p-RPS6 and p-4E-BP1 were markedly increased following PRMT4 overexpression, which indicated that PRMT4 may play an oncogenic role in HCC cells by activating the AKT/mTOR pathway. This evidence concerns the gene AKT1 and hepatocellular carcinoma.