Of note, mutation of several ALS-associated proteins, including superoxide dismutase 1 (SOD1), RNA-binding protein fused in sarcoma (FUS) and TAR DNA-binding protein 43 (TDP43; also known as TARDBP), have been reported to disrupt the secretory pathway, suggesting additional mechanisms linking defective traffic to ALS (Soo et al., 2015). Here, SOD1 is linked to amyotrophic lateral sclerosis.