Epigenetic events including histone acetylation have recently been reported to govern the expression of NIK in human cancers.7 Disruption of a closed chromatin structure by HDAC inhibitors has been described to lead to enhanced NIK expression and NF-κB activation.7 There exist several crosstalks between the canonical and the non-canonical NF-κB pathway.5 For example, NIK phosphorylates not only IKKα but also IKKβ, thereby activating both the non-canonical and canonical NF-κB pathway.6 Moreover, NIK has been reported to phosphorylate p65, which enhances its transcriptional activity.8 This evidence concerns the gene IKBKB and cancer.