We observed that either exogenous IκBα OE or NF-κB inhibitor BAY11-7082 treatment significantly abolished the effects of A20 KD on NPC cell proliferation and apoptosis, whereas exogenous p65 OE restored the effects of A20 OE on NPC cell proliferation and apoptosis (Figures 8a–c). The gene discussed is TNFAIP3; the disease is nasopharyngeal carcinoma.