As non-canonical signaling is frequently constitutively activated in several cancers, including MM and DLBCL, by recurrent genetic alterations, including NIK amplifications and c-IAP1/2 and TRAF3 deletions, NIK has emerged as an attractive target for therapeutic interventions, given its key role in controlling IKKα phosphorylation and NF-κB2/p100 processing [10]. Here, NFKB2 is linked to cancer.