Of clinical relevance, NOV/CCN3 depletion is a main driver of AR signaling and androgen-independent Castration Resistant Prostate Cancer (CRPC) progression and drug resistance; a significant decrease of NOV/CCN3 expression is observed in CRPC compared with localized prostate cancer in various prostate cancer patient cohorts [58]. This evidence concerns the gene CCN3 and prostate carcinoma.