Next, we investigated the possible mechanisms whereby mTORC1 is activated in HB. In this regard, a recent study suggested that YAP and TAZ regulate SLC38A1 and SLC7A5 expression in human HCC cells, leading to mTORC1 activation . Therefore, we tested the hypothesis that YAP and TAZ may function to regulate mTORC1 in an analogous manner in HB. For this purpose, we first determined the expression of amino acid transporters SLC38A1, SLC7A5, and SLC1A5 in normal liver and YAP/β-catenin-induced HB tissues. Connective tissue growth factor (CTGF), a well-known target of YAP, was used as positive control (Figure 4A). Importantly, we found that in YAP/β-catenin-induced HB tumors, only SLC38A1 expression was upregulated (Figure 4A). Next, we investigated whether amino acids were required for human HB cell growth and mTORC1 activation. For this purpose, Hep293TT and HepG2 cells were cultured in amino acid free medium (Figure 4B and 4C). Of note, we found that deprivation of amino acids strongly inhibited Hep293TT and HepG2 cell growth (Figure 4B), and it led to the reduction of mTORC1 activation, as indicated by decreased p-mTOR, p-S6K, p-RPS6, and p-4EBP1 levels (Figure 4C). Thus, the results support the hypothesis that amino acids are key activators of mTORC1 in HB cells.