Redox regulation is currently considered as a mode of signal transduction for coordinated regulation of a variety of cellular processes. The transcriptional regulation of gene expression is also influenced by cellular redox state, most possibly through the oxido-reductive modification of transcription factors. The glucocorticoid receptor belongs to a nuclear receptor superfamily and acts as a ligand-dependent transcription factor. We demonstrate that the glucocorticoid receptor function is regulated via redox-dependent mechanisms at multiple levels. Moreover, it is suggested that redox regulation of the receptor function is one of dynamic cellular responses to environmental stimuli and plays an important role in orchestrated crosstalk between central and peripheral stress responses.