In MM, several studies recently showed that TNF receptor-associated factor 3 (TRAF3) is an important target of deletion in this locus. TRAF3 is associated with negative induction of noncanonical NF-κB pathway, enhances BIRC2/BIRC3 mediated proteasome degradation of NF-κB inducing kinase (NIK), and thus increases autonomy of tumor PCs from the bone marrow microenvironment [29]. This evidence concerns the gene NFKB1 and Miyoshi myopathy.