Functional analyses revealed that, by suppressing SLC7A11 transcription, BAP1 inhibits cystine uptake and GSH biosynthesis and promotes ferroptosis under various ferroptosis-inducing conditions; furthermore, tumor growth suppression caused by BAP1 restoration in BAP1-deficient tumors can be partly abolished by SLC7A11 overexpression or treatment with ferroptosis inhibitor, and BAP1 mutations derived from human cancers abrogate their abilities to suppress SLC7A11 expression and to induce ferroptosis (Zhang et al., 2018b). The gene discussed is BAP1; the disease is neoplasm.