Several lymphoid cancers, particularly multiple myeloma but also Hodgkin lymphoma and cIAP2-MALT1 expressing MALT lymphoma (discussed in Section 4), harbor various genetic alterations which affect different regulators of the non-canonical NF-κB pathway and rely on constitutive nuclear activity of p52/RelB heterodimers [19,20,160,169,170]. This evidence concerns the gene NFKB1 and AL amyloidosis.