Since a key pathogenetic function of NF-κB in multiple myeloma is to upregulate genes that block apoptosis and, despite its ubiquitous nature, NF-κB signalling induces highly tissue- and context-specific transcriptional programs [6,11,12,14,79,192], we targeted an essential downstream effector of this pathogenically critical activity of NF-κB, in order to achieve cancer cell-selective therapeutic specificity and thereby circumvent the limitations of conventional IKK/NF-κB-targeting drugs. This evidence concerns the gene NFKB1 and AL amyloidosis.