This can occur at several levels: (i) simple overexpression of the AR gene [31,131]—a more reversible response to the changing microenvironment, (ii) alternative splicing of the AR mRNA to generate a truncated protein which can translocate to the cancer cell nucleus and activate gene expression in the absence of DHT ligand [33,127,128] or (iii) activation of a non-androgen-driven salvage pathway, as illustrated in Figure 2, but also by utilization of the glucocorticoid receptor (GR) protein [124]. The gene discussed is NR3C1; the disease is cancer.