AR and prostate carcinoma: We hypothesised that a mutant receptor activated by different agonists could therefore regulate different subsets of genes, hence we studied the expression levels of genes involved in prostate differentiation (Kallikrein 2, KLK2, and Differentiation Regulated Gene-1, DRG-1) and cell cycle progression (Cyclin Dependent Kinases 2 and 4, CDK2 and CDK4) in the LNCaP prostate cancer cell line, which endogenously expresses the T877A mutant AR [85].