A clear explanation for the high incidence of breast cancer in modern women is now possible. The risk of breast cancer rises steeply from menarche until menopause. Associated with the reproductive process, the ovary, including the corpus luteum, produces substantial amounts of estrogen and progesterone, both of which induce growth of the breast epithelium. This sex-steroid-driven breast epithelial cell proliferation increases the risk of carcinogenesis by accelerating the occurrence of somatic genetic errors. Postmenopausally, as there is little cell proliferation, the breast epithelium is more“resistant”to mutagenic effects, and breast cancer risk rises at a low rate. Unfortunately, the genetic errors accumulated during the premenopausal period are not lost following menopause, and breast cancer risk remains high. Sex-steroid antagonists, such as tamoxifen, may reduce breast cancer incidence both by blocking breast epithelial cell proliferation and by direct antitumor effects on clinically occult breast cancers. The rationale for a contraceptive designed to reduce breast cell proliferation by decreasing premenopausal sex-steroid exposure is presented.