Mechanistically, the PR-DUB complex binds on the SLC7A11 promoter, allowing BAP1 to deubiquitinate H2Aub on the SLC7A11 promoter and subsequently repress SLC7A11 expression independent of p53 (Fig. 2), resulting in decreased cystine uptake and increased ferroptosis sensitivity; conversely, BAP1 deficiency in cancer cells leads to SLC7A11 upregulation and ferroptosis resistance (Zhang et al., 2018b; Zhang et al., 2019c). This evidence concerns the gene SLC7A11 and cancer.