The availability of our novel CRPC xenograft and genetically matched AR+/AR-KO LNCaP clonal models should facilitate future studies on: (1) dynamic and reciprocal cooperation and interactions between the two PCa cell subpopulations during ADT and tumor relapse, (2) the causal functions of and novel signaling pathways in mediating Enza response by cytoplasmic AR (e.g., LAPC4 1° CRPC), and (3) PCa cell reprogramming and lineage plasticity accompanying tumor progression and clinical treatments. This evidence concerns the gene AR and neoplasm.