Androgen deprivation therapy (ADT) is the conventional firstline treatment for prostate cancer [1,2].Unfortunately,after initial response to this therapy,some cases finally inevitably progress to androgen-independent refractory prostate cancer within 18-36 months [3,4].During the conversion to androgen independence,the androgen receptor (AR)-mediated signaling pathway is irregularly reactivated and plays a center role [S].So far,multiple AR-related mechanisms have been recorded and contributed to androgen independence,including AR amplification/overexpression,mutations,activated alteative splicing variants,coactivators,ligand-independent activation,and androgen-independent protein isoform [5].However,the roles of two polymorphic trinucleotide repeats (CAG and GGC) within exon 1 of AR gene in the conversion to androgen independence are still inconclusive.