In summary, the reciprocal HBXIP/Nrf2 feedback loop promotes anoikis resistance in breast cancer cells both in vitro and in vivo by maintaining robust cellular ROS levels and Prdx1 stabilization, which inhibits the release of JNK1 from Prdx1-GSTπ-JNK1 heterotrimeric complexes and subsequently inhibits JNK activation (Fig. 7). This evidence concerns the gene PRDX1 and breast cancer.