Overactivation related mutations in NF-kB signaling molecules have been identified in the pathogenesis of MM [123]; overactive molecules in this pathway promote the growth of MM cells via expression of growth-promoting cytokines like IL-6, cell-cycle regulators that decrease cells’ sensitivity to cycle arrest, anti-apoptotic molecules, telomerase reverse transcriptase (TERT), angiogenic factors like VEGFs, and pro-adhesion molecules [123]. Here, NFKB1 is linked to Miyoshi myopathy.