In glioma or glioblastoma cells [6], [7], breast carcinoma cells [8], colon cancers [9], squamous cell derived tumors [10], prostate cancer cells [11]–[13] and melanomas [14], [15], targeting disruption of STAT3 activity by interfering RNAs, expressing dominant negative STAT3 forms or applying specific signaling inhibitors would remarkably down regulate STAT3 induced genes, including CyclinD1, Bcl-xl, c-Myc, Survivin and other genes regulating cell cycles and cell proliferation, and then subsequently reduce cell growth and enhance cell apoptosis [16], [17]. This evidence concerns the gene STAT3 and prostate carcinoma.