Furthermore, BACH1 stimulates p‐AKT and p‐p70S6K, leading to enhanced cyclin D1 expression, which facilitates the proliferation of ovarian cancer cells and transplanted tumors.[239] In another study, transcriptomic data was analyzed to develop a mechanism‐based gene regulatory network, revealing that Raf kinase‐B inhibitor protein (RKIP) and BACH1 belong to two antagonistic “teams”—BACH1 driving the promotion of EMT, stem‐like, and therapy‐resistant cell states, while RKIP enabling the promotion of epithelial, less stem‐like, and therapy‐sensitive phenotypes. This evidence concerns the gene PEBP1 and ovarian carcinoma.