Until now, ERG was suggested to modulate the phenotype of prostate cancer cells by a wide range of processes, including: disruption of AR signaling [10], activation of c-myc signaling [11] and estrogen receptor network [12], activation of the Wnt pathway and induction of epithelial-to-mesenchymal transition [13], promotion of cell invasion [14], physical interaction with PARP1 [15] and activation of TGF-β/BMP signaling [16]. The gene discussed is ERG; the disease is Familial prostate cancer.