These results demonstrate that TAK1 inhibition ameliorates inflammatory cytokine-induced myopathy via a suppression of the expression of a muscle atrophic factor, myostatin, and an enhancement of the expression of myogenic factor, MyoD1, with the increased expression of both fast-twitch and slow-twitch muscle proteins, and that TAK1 inhibition by LLZ also suppresses the degradation of muscle proteins via a reduction in the expression of E3 ubiquitin ligases, Atrogin-1, and Murf-1. Here, FBXO32 is linked to myopathy.