In certain cancer types, such as multiple myeloma, diffuse large B-cell lymphoma (DLBCL), Hodgkin’s lymphoma and glioblastoma multiforme (GBM), NF-κB is frequently stably activated by recurrent genetic alterations of upstream regulators of its pathway [6,11,12,13,14,15,16,17,18,19,20]. This evidence concerns the gene NFKB1 and AL amyloidosis.