The fate of steroid-receptor complexes after their nuclear retention in target cells is not firmly established. Nuclear glucocorticoid- and androgen-receptor complexes could be recycled back to the cytosol in their responsive tissues, whereas this has not been clearly established for the case of progesterone and estrogen receptors. The models of steroid receptor recycling proposed so far involve release of chromatin-bound complexes into the cytosol, loss of steroid, and receptor inactivation. These receptors, however, can eventually be reactivated to a steroid binding form to reinitiate a cycle of steroid binding and further nuclear translocation. We propose that this model can represent a general aspect of steroid hormone action, provided that inactivation/reactivation processes occur in every steroid responsive system. A process involving a reversible receptor inactivation could play a major role in the control of steroid receptor recycling. It is proposed that a control on the extent of receptor available to steroid binding could result in a modulation of cellular responses to steroid hormones.