Abstract: Hormone receptors and the transcription factor Jun/AP-1 have been shown to reciprocally repress one another by a mechanism which is independent of DNA binding. For example, over-expression of AP-1 represses glucocorticoid-induced activation of genes carrying a functional glucocorticoid response element. Conversely, glucocorticoid has been shown to repress the transcriptional activation of genes which are controlled by promoters which contain the AP-1 binding site. In addition, methods are disclosed for selecting compounds useful for treating cells undergoing uncontrolled proliferation, such compounds being capable of disrupting the function of AP-1, but display substantially no ability to promote the transcriptional activation of hormone responsive genes.