Based on studies with MMCLs, some of the NFkB mutations in MM tumors and MMCLs activate mainly the classical pathway (CYLD, NFKB1, TACI), and one mainly the alternative pathway (NFKB2), but most activate the alternative and to a lesser extent the classical pathway (cIAP1/2, NIK, TRAF2, TRAF3, CD40) (Fig.2B). This evidence concerns the gene NFKB2 and Miyoshi myopathy.