On the other hand, deletion of NIK suppresses tumor formation in mouse model.392 Besides, rearrangement or mutations of NF-κB2 have also been found in various human malignancies, including multiple myeloma, T-cell and B-cell lymphoma, with constitutive processing of p100, resulting in sequential non-canonical NF-κB activation.396–398 Understanding of these mechanisms is subjected to provide crucial information for discovery of new therapeutic targets for direct suppression of tumorigenesis and tumor growth, as well as to optimize tumor immunotherapy by inducing TLO formation. The gene discussed is NFKB1; the disease is AL amyloidosis.