In other types of cancer, the AKT pathway is persistently activated as a result of mutation of AKT itself or its upstream pathways of growth factors36, which would phosphorylate CASTOR1 leading to its ubiquitination and degradation, and activation of mTORC1 regardless of the presence of high or low level of arginine (Supplementary Fig. 12c, d). Here, CASTOR1 is linked to cancer.