These results suggest that after the acquisition of oxidative stress resistance, similar to the response of C4–2 mCRPC cells, LNCaP-HPR cells increased the level of p-NF-κB after Cab treatment, indicating that NF-κB inhibition might be a therapeutic strategy for enhancing Cab sensitivity in aggressive PC cells. The gene discussed is NFKB1; the disease is pachyonychia congenita.