NFKB1 and Miyoshi myopathy: There are several hypotheses for the mechanism of action of these agents in MM, including: accumulation of incompatible regulatory proteins within the cell [15]; accumulation of mis-folded proteins from the endoplasmic reticulum (“ER stress”) which trigger an unfolded protein response that leads to suspension of protein synthesis [15,16,17]; and inhibition of NF-κβ signaling pathway (critical for the coordination of cellular responses to stress/inflammation) via interference with degradation of proteins that inhibit NF-κβ (Iκβ) [18].