To interpret this observation in the context of prostate cancer genomics, we hypothesized that ERG fusion may be driving the expression of PCA3. However, PCA3 displayed a bimodal distribution in both ERG+ and ERG- tumors, as determined previously by our group [19], suggesting that the observed bimodal distribution is independent of ERG expression (Figure 1D). The gene discussed is ERG; the disease is prostate cancer.