Given that T3 could activate the AMPK/Raptor pathway, inhibiting the PI3K/Akt/mTOR-induced HIF-1α nuclear translocation, which has been implicated in lenvatinib resistance [47, 48], this study hypothesized a synergistic effect of T3 and lenvatinib in HCC treatment. The gene discussed is MTOR; the disease is hepatocellular carcinoma.