ERG is commonly over-expressed in PCa (~50–55% of cases), most often due to fusions with the androgen-responsive TMPRSS2 promoter.6 ERG is considered a major driver of PCa and is thought to be responsible for many PCa cell traits.4 Androgen deprivation therapy (ADT) is a widely used approach to prevent disease progression.39 However, nearly all prostate cancers eventually become resistant to ADT,40 meaning that there is a clinically unmet need for new therapies targeting the inappropriate activation of ERG due to TMPRSS2 fusions. The gene discussed is TMPRSS2; the disease is prostate cancer.