Additionally, Sema3A-CRMPs signaling has been suggested to be involved in ALS pathogenesis because Sema3A is upregulated in the motor cortex of ALS patients and the terminal Schwann cell adjacent to neuromuscular junctions (NMJs) in SOD1G93A mice (De Winter et al., 2006; Körner et al., 2016). This evidence concerns the gene SEMA3A and amyotrophic lateral sclerosis.