In support of targeting both ER and PR as a treatment approach to breast cancer, our past studies demonstrated that 4-OHT and MIF more effectively induce growth arrest and cell death than do either 4-OHT or MIF treatment of ER+PR+, antiestrogen-sensitive [13,14], and ER+PR+, antiestrogen-resistant breast cancer cells [17]. The gene discussed is MIF; the disease is breast cancer.