The data support the notion that ERG regulation of androgen synthesis in cancer cells leads to activation of AR as shown by AR responsive gene expression and this process is amenable to AR inhibition through enzalutamide for in vivo tumor growth, whereas when ERG factor is downregulated, intracellular androgen synthesis is downregulated and AR is no longer active (as shown by lower AR responsive gene expression), thus, not allowing anti-AR inhibitor enzalutamide to exert to growth inhibition to the extent of inhibition observed with ERG intact tumors (Fig. 5). The gene discussed is AR; the disease is cancer.