As a result, GR acts as a regulator that can increase OXPHOS and mitochondrial adenosine triphosphate production when the cells need it.[55] It is known that the upregulation of OXPHOS can confer resistance to androgen ablation.[59–61] These findings suggest that in prostate cancer under antiandrogen treatment, the mitochondrial GR translocation might have prosurvival effects and contribute to treatment failure. The gene discussed is NR3C1; the disease is prostate cancer.