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). The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.