In sum, TAK1-inhibitors can target MM cells in several manners: i) directly shifting constitutively- or melphalan-activated TAK1 from NF-κB/MAPK activation to cell death, ii) reducing activity of survival factors such as MYC and E2F, and iii) neutralizing the melphalan-induced UV-response. Here, NFKB1 is linked to Miyoshi myopathy.