Given that constitutively active androgen receptor splice variants, in particular AR-V7, have been shown to confer resistance to abiraterone or enzalutamide [13,14], and that activation of NF-κB [24,25] and reactivation of AR signaling [26,27] are involved in prostate cancer progression and CRPC development, it would be of interest to investigate any interactions among AR-V7, NF-κB, and melatonin in prostate cancer cells to gain further insights on the therapeutic potential of melatonin in advanced prostate cancer and CRPC management. The gene discussed is AR; the disease is prostate cancer.