Half of all prostate cancers contain an oncogenic gene fusion between the androgen-regulated upstream elements of the TMPRSS2-gene with the consequently upregulated ETS transcription factor ERG. Despite this high prevalence, detecting the presence of TMPRSS2-ERG in patients tumors has little-to-no useful clinical utility, in part due to a lack of understanding of its mechanisms of oncogenesis. I have characterized a gene, ERF, which functions as a putative tumor suppressor. I had hypothesized that ERF is outcompeted by the TMPRSS2-ERGgene product. Currently, we have identified how ERF and ERG may compete with each other, and as a result, have opposing effects on cancer cell proliferation. I am currently now investigating the tumor suppressor function of ERF in prostate cancers lacking TMPRSS2-ERG.