Although still dependent on the androgen/androgen receptor axis, most prostate cancers progress to a castration-resistant phenotype that is due, in part, to intratumoral and adrenal synthesis of androgens, overexpression and mutation of the androgen receptor, expression of AR splice variants, stabilization of AR by chaperones, and androgen-independent activation of the receptor by growth factors and intracellular signal transduction pathways [23, 24]. The gene discussed is AR; the disease is Familial prostate cancer.