Importantly, from a mechanistic standpoint, it is also unclear that the clinical response to proteasome inhibitors in patients with multiple myeloma and other B-cell malignancies results from the inhibition of NF-κB signalling, as it is becoming increasingly clear that the cellular accumulation of undigested proteins in these immunoglobulin-producing tumours can activate the unfolded protein response (UPR), thereby accelerating tumour-cell death [162]. The gene discussed is NFKB1; the disease is AL amyloidosis.