Our findings suggest yet another consideration that adds to the complexity of glucocorticoid signaling in prostate cancer, namely susceptibility of the administered glucocorticoid to metabolic inactivation, that is likely relevant to the increased GR expression that may occur alongside enzalutamide resistance and allows direct tumor-promoting effects of glucocorticoids in CRPC. The gene discussed is NR3C1; the disease is prostate carcinoma.