Interestingly, a number of genetic alterations promoting NIK stabilization and p100 processing, such as c-IAP1/2 and TRAF3 deletions and NIK amplifications, have been reported in multiple myeloma, where they drive constitutive NF-κB activation and multiple myeloma cell survival [21,24,26,28,34,68,92]. Here, NFKB1 is linked to AL amyloidosis.