The experimental results show that, compared with PLC5 cells that had not undergone long-term LPS exposure, TLR4-mediated signaling, including Akt and p38, in PLC5 cells with long-term LPS exposure was activated in response to LPS stimulation for 30 min (Figure 5G), indicating that long-term LPS stimulation to mimic the chronic inflammatory environment is able to promote TLR4 expression and sensitize TLR4-induced signals in HCC cells. Here, AKT1 is linked to hepatocellular carcinoma.