Keats et al. identified a promiscuous array of mutations that result in the constitutive activation of the non-canonical NF-κB pathway in approximately 20% of MM patients (inactivation of TRAF2, TRAF3, CYLD, cIAP1/cIAP2, and activation of NFKB1, NFKB2, CD40, LTBR, TACI, and NIK) [72]. The gene discussed is CD40; the disease is Miyoshi myopathy.