NFKB1 and AL amyloidosis: Recently, genetic alterations in components of the noncanonical and canonical NF-κB pathways (e.g., NIK, TRAF3, CYLD, BIRC2/BIRC3, CD40, NFKB1, or NFKB2) resulting in their activation have been identified in multiple myeloma [19], [20].