Furthermore, we analysed regulators of atrophy pathways in the skeletal muscle, such as the muscle-specific E3 ubiquitin ligases MURF1 and MAFbx/Atrogin-1, and found an increase in ALS samples (Supplementary Fig. 2e), suggesting an activation of the ubiquitin/proteasome system, leading to protein degradation. This evidence concerns the gene TRIM63 and amyotrophic lateral sclerosis.