It is uniequivocal that prolactin is an influential hormone in murine mammary tumorigenesis. The Berenblum hypothesis, a well-known theoretical model of tumorigenesis that depicts this oncogenic process as a 2 step mechanism, i.e., initiation and promotion, is a conceptual scheme in which the action of prolactin in mammary tumorigenesis may be understood. According to this conceptual model, prolactin would participate in the initiation and promotion steps of mammary tumorigenesis. In the initiation phase, variations in prolactin secretion appear to influence the metabolism of the mammary epithelium, so that the epithelium would be more receptive to or refractory to an initiating agent (e.g., chemical carcinogens, physical carcinogens, oncogenic viruses, etc.), i.e., a permissive action. In the promotion phase, prolactin may act as a promoter or an antipromoter of the transformed mammary epithelium. In promotion, the hormone may directly or indirectly (via the ovary) stimulate mitotic activity of the transformed epithelium. In antipromotion the hormone, in the presence of requisite hormones (e.g., glucocorticoids), may synergistically induce differentiation (e.g., lactation) in the transformed epithelium. A tumor would result in the former (promotion) but not in the latter (antipromotion) case. Whether or not prolactin is significantly influential in human breast tumorigenesis remains to be determined. This is an extremely important area of research which is justifiably receiving increased attention. If prolactin can be shown to influence human breast epithelium in a manner similar to its effect on rodent mammary tissue, prophylactic and/or chemotherapeutic control of human breast tumorigenesis may be feasible by appropriate drug mediated prolactin suppression.