Considering these observations and the high homology between ETV1 and ETV4 (defined by their DNA binding motif), we questioned whether these PEA3 family members would cooperate or have redundant roles in prostate carcinogenesis, by regulating the same or distinct target genes and pathways, and whether in vitro models of ETV1 and ETV4 overexpression could reveal markers of tumor aggressiveness. The gene discussed is ETV4; the disease is prostatitis.