Furthermore, our data suggest the functional redundancy of YAP and its paralog TAZ in regulating SLC38A1 expression and mTORC1 activity in human HB cells. While the relevance of YAP in HB is underscored by a body of experimental evidence, including the findings from the present study, there is no study on the role of TAZ in this tumor type. Our results support the possible involvement of TAZ in HB, and this issue clearly warrants further studies. In particular, it would be highly important to determine whether YAP and TAZ, besides SLC38A1 and mTORC1, regulate the same or distinct pathways in HB.