Our data demonstrated the following: (i) patients with higher levels of FXR appear to have greater survival, but only in ER− and basal-like subtypes, not ER+ or luminal A subtype; (ii) human and murine BC cell lines express FXR; (iii) the FXR agonist OCA slowed tumor progression in a murine model, potentially through downregulation of the MYC pathway leading to decreased expression of the oncogenic transcription factor MAX; (iv) in vitro OCA demonstrated potent dose-dependent inhibition of proliferation and migration, as well as reduced viability. Here, MAX is linked to neoplasm.