Several major signalling pathways have been implicated in the pathogenesis of MM including the JAK-STAT3, PI3K/Akt/mTOR, and NF-κB pathways [62,63], wherein STAT3 might be constitutively active or may be activated by the interleukin-6(IL-6)-JAK-STAT3 axis in MM [64]. This evidence concerns the gene NFKB1 and Miyoshi myopathy.