Prior studies have suggested that p100, instead of being partially proteolysed into p52, undergoes complete degradation in myeloma-derived cells in the presence of chronic non-canonical signal.29, 30 As RelB:p52 constituted only a minor NFκB DNA-binding activity in KMS28PE and JK6L cells (Figure 2b), we examined whether activating mutations in the non-canonical module led to degradation of p100. The gene discussed is RELB; the disease is plasma cell myeloma.