Clinical trials using bortezomib alone in advanced stage prostate cancer and in combination with androgen blockade and chemotherapy showed limited clinical efficacy due to incomplete targeting of NF-ĸB/Rel subunits and other signaling pathways mediated through androgen receptor and β-catenin, which contribute to the resistance to bortezomib and castration in prostate cancer [17, 18]. The gene discussed is REL; the disease is prostate carcinoma.