Specifically, mutations in SOD1 have been found to affect trafficking at the Golgi through two mechanisms: the ALS-associated mutations SOD1A4V, SOD1G85R, and SOD1G93A disrupt the secretory pathway, while the SOD1A4V mutation triggers endoplasmic reticulum (ER) stress causing the accumulation of secretory proteins and apoptosis [20], as presented in Figure 1. Here, SOD1 is linked to amyotrophic lateral sclerosis.