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. This evidence concerns the gene NFKB1 and prostate carcinoma.