Zhou et al. showed that pharmacological targeting of IAPs suppressed NF-κB activation and induced FADD-dependent apoptosis in multiple myeloma (MM) cells, and cells expressing dominant-negative FADD were markedly less sensitive to IAPs inhibitors, highlighting the significant functional contribution of FADD in targeting anti-apoptotic NF-κB activation [122]. The gene discussed is NFKB1; the disease is Miyoshi myopathy.