In summary, inhibiting EGFR by the overexpression of endogenous EGFR suppressors such as miRNA-133b, METTL14, and YTHDF2 led to the subsequent inactivation of the downstream PI3K/AKT/mTOR signaling pathway and effectively reduced the malignancy of HCC cells by inducing cell apoptosis and suppressing cell proliferation. This evidence concerns the gene MTOR and hepatocellular carcinoma.