On one hand, the dephosphorylation of these intracellular mediators of the INS can activate the Forkhead box class O (i.e., FoxO), leading to transcription of several components of the ubiquitin-proteasome (UPS; Atrogin-1/Mafbx32 and MuRF1/Trim63) and autophagic-lysosomal (ALS; Map1lc3b and Gabarapl1) systems, which degrade most cellular proteins and organelles in skeletal muscle (Yang et al., 2008; Milan et al., 2015). This evidence concerns the gene TRIM63 and amyotrophic lateral sclerosis.