Several years ago, our group identified genomic rearrangements in prostate cancer resulting in the fusion of the 5’ untranslated end of TMPRSS2 (Transmembrane serine protease 2; a prostate-specific gene controlled by androgen) to members of the ETS (E26 transformation-specific) family of oncogenic transcription factors, leading to the over-expression of ETS genes like ERG (ETS-related gene), ETV1 (ETS variant transcription factor 1), ETV4 (ETS variant transcription factor 4), and others, with ERG being the most common gene fusion partner [3]. The gene discussed is ETV4; the disease is prostate cancer.