Since shRNA-mediated knockdown of the alternative NF-κB subunits RELB or p52 in MM lines, as expected, was reported to cause cell death [74,85], the findings by Annunziata et al. suggest that both NF-κB pathways are active and promote cell growth/survival in MM in cases with genetic mutations, leading to constitutive NIK expression (which comprise a major fraction of NF-κB-mutated MM cases). This evidence concerns the gene MAP3K14 and Miyoshi myopathy.