Since most prostate cancer-prevalent fusion genes are formed by the fusion with the androgen-responsive promoter region of the androgen-activated genes (e.g., TMPRSS2 and SLC45A3), it is thus generally regarded that these fusion genes are mainly regulated by androgen receptor (AR) [1] and their oncogenic activation or overexpression is attributed to the activation of AR signaling in androgen-dependent prostate cancer. This evidence concerns the gene AR and Familial prostate cancer.