Furthermore, currently approved antiandrogens, such as bicalutamide, hydroxyflutamide and nilutamide, have weak agonistic effects in prostate cancers with mutated or overexpressed AR (Chen et al, 2004), and this provides a mechanistic explanation for the treatment failure using these agents as well as the clinical phenomenon of the ‘androgen withdrawal response’. The gene discussed is AR; the disease is prostate carcinoma.