Corticosteroids induce apoptosis in both normal and neoplastic lymphocytes. For this reason they are commonly used to treat autoimmune disorders and lymphoid malignancies also. The exact mechanism of corticosteroid-induced apoptosis is not fully understood despite the fact that much has been found in respect to several supposed involved mechanisms. This process is arbitrarily divided in several phases. Firstly, glucocorticoid enters the cell and binds to the glucocorticoid receptor (GR) in the cytoplasm. The GR changes conformation and the heat shock proteins, normally bound to the receptor in the steady state, fall off. The activated GR-hormone complex enters the nucleus and binds to its specific DNA binding site, the glucocorticoid responsive element (GRE), thus resulting in activating or repressing transcription of genes. The activation of caspases or other proteases and endonucleases finally results in the commitment to cell death.