Ever since it was discovered in the 1940s that androgens promote prostate cancer growth, testosterone suppression has been the mainstay of therapy for metastatic prostate cancer.1 Initially, this was achieved by surgical removal of the testicles and later by medical therapy with blocking luteinizing hormonal–releasing hormonal therapy. The advent of medical therapy allowed the ability to suppress testosterone and then hold dosing to allow recovery of testosterone levels, and patients could then be redosed when the cancer recurred with testosterone recovery. There was an initial thought that this “intermittent” dosing might prolong the efficacy of this therapy2 as well as lead to a better quality of life. Improved life quality is especially relevant given the myriad adverse effects of testosterone suppression, including hot flashes, weight gain, mood disturbance, and fatigue over a long duration of therapy for many men—especially after the advent of the prostate-specific antigen (PSA) test and treatment of patients with only biochemical evidence of disease recurrence after prostatectomy or radiation therapy.