The interaction of androgen receptor (genotoxic stress) and activation-induced cytidine deaminase (AID) (transcriptional stress) is likely to be the cause of the double-strand breaks that drive the specific changes in the genome and/or the chromatin remodeling that bring a TMPRSS2 into proximity with ETS genes to form gene fusions (TMPRSS2-ERG, TMPRSS2-ETV1, and SLC45A3-ETV1) in prostate cancer [24, 139, 140]. This evidence concerns the gene ERG and prostate carcinoma.