KRAS and hepatocellular carcinoma: Single inhibition of Mek/Erk could significantly reduce the activation of mTOR and its downstream targets p-4EBP1Thr37/46 and p-S6Ser235/236, and this effect was much stronger than the inhibitory effect of PI3K/Akt, suggesting that mutant Kras promoted Tsc1 insufficiency-driven mTOR activation mostly via Mek/Erk signaling in HCC tumorigenesis (Figure 2D-E).