In summary, our data indicate that i) NF-κB activation in the BM is mild and heterogeneous, ii) is due to the activation of a minority of cells, iii) is dampened by restraining physical microenvironmental cues and iv) can be triggered by IL-1β-dependent stroma-to-MM crosstalk and can be reduced by treatment with Anakinra. This evidence concerns the gene NFKB1 and Miyoshi myopathy.