For example, ARID1A-deficient cancers respond to PARP inhibitors due to ARID1A’s role in DNA repair; ATR/ATM inhibitors are synergistic in cancers with ARID1A-deficiency or BAF-inhibition, and cancers with PBRM1, BRD7, or BRD9 inactivation are sensitive to replication stress and can be treated with PARP and ATR inhibitors (Shen et al., 2015; Williamson et al., 2016; Hu et al., 2019; Chory et al., 2020; Zhou et al., 2020; Chabanon et al., 2021). The gene discussed is PBRM1; the disease is cancer.