Notably, the inactivated NF-κB signaling in NPC53 cells by transcriptome characterization suggests the important roles of EBV infection and its encoded genes in driving NF-κB signaling, and indicates that mutations in TRAF3 and CYLD could be essential but not sufficient for the induction of potent NF-κB signals in NPC cells. The gene discussed is CYLD; the disease is Epstein-Barr virus infection.