Finally, to deduce a molecular mechanism to account for differential gene expression patterns for each gene-set, we analyzed copy number variation of a CGH array dataset, for the patients used for our GSEA and survival prediction outcome. For the White gene-set 2, we were able to confirm that patient survival based on the Neosperidin-dihydrochalcone criteria of PSA value, Gleason score and combined, was dependent on copy number variation. This was the only gene-set that was predictive for survival outcomes based on copy number variation. Knowledge of various molecular mechanisms of action contribute to our understanding of wild type AR function. Most mechanisms require the involvement of ligand binding and interacting partners. Examples of this include AR interactors involved in gene transactivation, including HSP70, HSP90, p300 and components of the RNA polII complex. Gain-of-function somatic mutations, abundant in cancerous tissues, typically add new functions, adding to the complexity of physiological and disease outcomes. We investigated the T877A-AR mutation, as it represents the most common AR mutation in clinical CaP specimens, and is the AR mutation found in the most studied prostatic cancer cell line, LNCaP. Mutations like T877A-AR, and several others in the ligand-binding domain of the receptor, allow the AR to bind to other classes of steroid ligands such as estradiol, dexamethasone and progesterone, including anti-androgens such as CPA, resulting in subsequent AR dependent gene transactivation. It is also now clear that as cancers evolve through many somatic mutations and undergo selection processes induced by classical drug therapies themselves. Futhrermore, a number of Benzoylpaeoniflorin studies have used LNCaP cells as a model for studying the progression from androgen-dependent to �Cindependent/ castrate resistant prostate cancer state and support the hypothesis that continuous AR activity and signaling continues to be one of the most important mechanisms in CRPC.These studies have substantiated extensive genetic alterations that range from single missense mutations, to copy number variations, splicing variants, genetic rearrangements and short DNA alterations in a large number of genes and AR cofactor interactions to reproduce androgen-independent scenario.