The transgenic mouse has emerged as an important model system to assess the transforming potential of oncogenes in the mammary epithelium. Mammary gland-specific expression of oncogenes in transgenic mice has resulted in the induction of a variety of phenotypes ranging from benign epithelial hyperplasias to metastatic mammary tumors. The induction of tumors in most of these transgenic models is a multi-step process where transgene expression, although required, is not sufficient for conversion of the primary mammary epithelial cell to the transformed phenotype. While the identity of many of these collaborating genetic events is obscure, several approaches have been applied with might shed light on their nature. In a few exceptional transgenic strains, tumor progression can occur very rapidly suggesting that, if additional genetic events are required, they occur very frequently. Recent genetic and biochemical characterization of these strains offers insight into the molecular mechanisms that may underlie the complex phenotypic features exhibited by these transgenic strains.