Pathways, such as tyrosine kinase signaling, which regulates muscle repair via IGF-1 (Schiaffino & Mammucari, 2011), and RNA degradation which is linked to TDP-43-mediated RNA processing defects (Buratti et al., 2010), further highlight key mechanisms driving muscle atrophy and dysregulation in ALS. Here, IGF1 is linked to amyotrophic lateral sclerosis.