Whereas in certain malignancies, such as multiple myeloma, diffuse large B-cell lymphoma (DLBCL), mucosa associated lymphoid tissue (MALT) lymphoma and glioblastoma multiforme (GBM), NF-κB is often constitutively activated by recurrent genetic alterations targeting upstream components of the NF-κB pathway, in the large majority of solid tumours and certain haematological malignancies, such alterations of the NF-κB pathway are relatively infrequent (DiDonato et al., 2012; Annunziata et al., 2007; Keats et al., 2007; Pasqualucci et al., 2001; Bredel et al., 2011). This evidence concerns the gene NFKB1 and AL amyloidosis.