Steroid hormones have well documented stimulatory and inhibitory effects on target cell proliferation. These effects are steroid- and target cell-specific and are mediated by cell cycle phase-specific actions. The molecular mechanisms by which steroids control rates of cell cycle progression are, however, not well defined. Recent advances in our understanding of cell cycle control by proto-oncogenes, tumor suppressor genes and cyclin dependent kinases provide models for further delineating the molecular basis of proliferation control by steroids. Transcriptional activation of c-fos, c-myc and cyclin D1 by estrogens and progestins in breast cancer cells and inhibition of expression of these genes by antiestrogens provide a paradigm for further understanding cell cycle control by steroids.