In this study, we show that cyst(e)ine not only promotes GSH biosynthesis, but also promotes GPX4 protein synthesis through activating mTORC1 (in this manuscript, we use the term “cyst(e)ine” to refer to “cystine and cysteine”), and that mTORC1 inactivation sensitizes cancer cells to ferroptosis by decreasing GPX4 synthesis, therefore revealing a crosstalk between mTORC1 and ferroptosis. Here, GPX4 is linked to cancer.