Prostate cancer is an androgen receptor-dependent disease, and therefore blockade of the androgen receptor has been an important tool in the treatment of this disease. However, although most patients benefit from androgen deprivation therapy, tumors inevitably continue to progress after one to four years due to multiple factors; once the cancer enters a state of “depot resistance”, it is a death knell for the patient. Early detection of metastatic prostate cancer by imaging and timely debulking treatment is beneficial to patients, and the use of new technologies has increased the time to progression to the end stage. Although detailed data are not yet fully available, the time from detection of metastatic cancer to patient death may now be more than 5 years. Previous studies have suggested that post-depression androgen resistance only occurs when the tumor progresses; however, the current study suggests that androgen receptors may remain activated even when testosterone concentrations remain at depressed levels (less than 50 ng/dl). Thus, controlling the expression of androgen receptors in the gland and tumor after denervation is critical for patients with metastatic prostate cancer. As described in this issue of NEJM, abiraterone acetate relies on selective inhibition of CYP17, a key enzyme in testosterone synthesis, to inhibit extra-gonadal androgen synthesis; and its significant effect in patients with advanced prostate cancer is also reported in detail in this article. The results of this study again demonstrate that metastatic prostate cancer remains highly androgen-dependent. However, there is a lack of data to support the efficacy of abiraterone in combination with other drugs, and further trials are needed to determine the effect of this drug in patients with different stages of prostate cancer. Until a few years ago, the only treatments available to extend the life span of patients with destructive resistance were paclitaxel (FDA-approved first-line chemotherapy for metastatic prostate cancer in 2004) and the earlier FDA-approved mitoxantrone (which improved the quality of life of patients). It was not until 2010 that the FDA approved two additional treatments, the autoimmunotherapy product prostate cancer vaccine Provenge (sipuleucel-T, for patients with no or minimal symptoms) and Jevtana (cabazitaxel, for patients whose disease has progressed again after chemotherapy with polyene paclitaxel). In addition, denosumab (denosumab) has been cleared by the FDA for its ability to prevent the incidence of skeletal-related events in patients with metastatic debulking-resistant prostate cancer. During the current study, there are still a number of issues that deserve our attention and consideration. First, how are patients who have and have not received chemotherapy treated during the drug trial? If they have the same stage of disease, can they be assigned to the same trial group? Second, the results of many drug trials have shown “significant” effects of the drug, so is it still in line with the humanitarian spirit to continue to use placebo as a control when conducting clinical drug trials? How to select the appropriate drug control? Although there are now relatively many treatment options for metastatic debulking-resistant prostate cancer, we have to admit that progression-free and overall survival rates are still relatively low with these treatments. However, as our understanding of the mechanisms involved in metastatic prostate cancer progresses, it is expected that in the near future, more effective treatments will be available to further improve the prognosis of patients with advanced prostate cancer; more clinical, imaging, and genetic targets will be identified and discovered, and they will replace some of the currently used clinical criteria and give patients individualized treatment plans.