Previous studies have identified STAT5A/B to be a critical survival factor in prostate cancer cells [23], and have further demonstrated increased STAT5A/B immunostaining in high-grade and CR clinical prostate tumors [24], [25], that active STAT5A/B in primary prostate cancer is predictive of early CR disease [26], and that transcriptional synergistic interaction between STAT5A/B and the androgen receptor inhibits apoptosis and promotes growth of prostate cancer cells in vitro[25]. Here, AR is linked to prostate neoplasm.