Collectively, these data suggest that although TMPRSS2-ERG fusion and loss of NKX3. 1 are among the most common mutational events found in prostate cancer, and although each of them can sensitize prostate epithelial cells for cooperating with other oncogenic events, these two events themselves do not appear to cooperate at a significant level in vivo to enhance prostate tumorigenesis. This evidence concerns the gene TMPRSS2 and Familial prostate cancer.