Pro‐inflammatory mediators such as TNF‐α, but also hyperammonemia, activate nuclear factor ‘kappa‐light‐chain‐enhancer’ of activated B cells (NF‐κB) signalling and induce, in part mediated by myostatin, downstream target genes including MuRF‐1 and atrogin‐1 (MAFbx) that promote muscle protein degradation through the proteasomal pathway.53, 54. The gene discussed is FBXO32; the disease is Hyperammonemia.