Multiple and recurrent genetic abnormalities in genes encoding regulators of the alternative NF-κB pathway (e.g. loss-of-function mutations in TRAF2/3 and cIAP1/2, gain-of-function mutations in NIK, and C-terminal truncation of p100) have been identified in MM cell lines and patient samples [31], [32], suggesting the involvement of the alternative NF-κB pathway in MM pathogenesis. The gene discussed is NFKB2; the disease is Miyoshi myopathy.