Nuclear factor κB (NF-κB) constitutive activation, which is related to both MM cell activity and BTZ resistance, hinges on the activity and degradation of inhibitor of kappa B alpha (IκBα).[47] NCTD can augment the antimyeloma effects of BTZ and impede the growth of MM cells by suppressing the activity of I-kappa-B kinase alpha (IKKα) and phosphorylation of IκBα, leading to an increase of IκBα and subsequent inhibition of constitutive NF-κB activation. The gene discussed is NFKBIA; the disease is Miyoshi myopathy.