It has been postulated that cross-talk between STAT3 and the androgen receptor plays a role in the development and maintenance of the hormone-refractory state in prostate cancer [47]; our data indicate that persistently-activated STAT3 may obviate the need for expression of the androgen receptor, since the androgen receptor did not respond to either DHT or F in S3c-transfected BPH-1 cells (Table 2). This evidence concerns the gene STAT3 and benign prostatic hyperplasia.