Consequently, we theorize that a trace amount of nuclear p65 is sufficient to promote tumorigenicity; p65 may have cytoplasmic functions that favor the cytoplasmic retention of p65 in NPC; cytoplasmic p65 expression is correlated with NPC progression; de novo expression of IκBα is an instant feedback mechanism that efficiently inactivates p65 in a temporal and spatial manner. Here, NFKBIA is linked to nasopharyngeal carcinoma.