Importantly, Sema3A was found to be upregulated in terminal Schwann cells of the SOD1G93A transgenic mouse model for ALS and in the motor cortex of ALS patients (De Winter et al., 2006; Körner et al., 2016), suggesting that it plays a toxic role in disease pathology and progression. Here, SEMA3A is linked to amyotrophic lateral sclerosis.