HB is a malignant form of liver cancer occurring in infants and children [1, 2]. Similar to other tumor types, multiple genetic alternations are likely to be required for the development of HB. In particular, somatic mutations of the CNNTB1 gene leading to the activation of Wnt/β-catenin signaling cascade, are a well-documented major driver genetic event in HB development [4, 5]. A recent body of evidence indicates that YAP is another, pivotal factor commonly activated in HB . In particular, it has been shown that concomitant activation of β-catenin and YAP results in HB formation in mice . Also, silencing of YAP and/or β-catenin leads to decreased proliferation of HB cell lines . However, the precise mechanisms by which YAP promotes HB development are not known. In this study, we demonstrate that mTORC1 is activated in both human HB cell lines and mouse YAP/β-catenin-induced tumor tissues. The importance of the mTORC1 pathway along HB development is underscored by the finding that inhibition of mTORC1 by either MLN0128 treatment or ablation of Raptor strongly suppresses HB occurrence in mice. Furthermore, we showed that YAP and its paralog TAZ regulate the expression of the amino acid transporter SLC38A1 in human HB cell lines, leading to mTORC1 activation (Figure 8). Our investigation therefore provides novel mechanistic insight into how YAP and TAZ may contribute to HB formation.