Publisher Summary This chapter discusses the regulation of mouse mammary tumor virus (MMTV) expression by glucocorticoids that have proved to be a very productive model for hormone action. Gene transfer experiments with fusions between MMTV and a variety of selectable genes have permitted for the first time the unambiguous identification of a cis-acting hormone regulatory sequence. The transfer of hormone responsiveness to genes that confer a phenotype observable at the cellular level now permits a variety of genetic approaches to be applied to the study of hormone action that were not previously available. Selection for the reversion of the inducible phenotype should permit the identification of variants in the hormone response pathway. Characterization of such lesions should provide a more detailed understanding of poorly understood processes, such as hormone-receptor complex activation, nuclear translocation, and chromatin binding, and may lead to the identification of previously unknown elements in the pathway. Directed mutagenesis with the increasingly powerful in vitro recombinant DNA techniques should permit the ultimate definition of sequences involved in the regulatory site at the nucleotide level.