Ductal growth during puberty is stimulated by estrogens, which elicit their effects via specific estrogen receptors, ER alpha and ER beta. Analysis of mice with targeted disruption of ER alpha or ER beta has emphasized the importance of ER alpha in mammary gland development. In the mouse mammary gland, ER alpha are expressed in both epithelial and stromal cells (Kurita and Cunha, unpublished), which raises the possibility that the growth and morphogenetic effects of estrogen could be mediated via either epithelial or stromal ER. The aim of this paper is to review the role of epithelial versus stromal ER in mammary ductal-alveolar growth to assess the importance of paracrine mechanisms.