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. This evidence concerns the gene NR3C1 and Familial prostate cancer.