The development and progression of CRPC is characterized by continued AR signaling, either through overexpression of the AR by gene amplification; mutations of the AR ligand binding domain (LBD); tumor-derived androgen production; expression of constitutively active AR splice variants (AR-SVs), of which AR-V7 remains the best studied; or co-regulator overexpression, including the transcription factor co-activator proteins p300/CBP [45,119]. The gene discussed is AR; the disease is neoplasm.