We recently demonstrated that Golgi-associated vesicular trafficking is inhibited in cells expressing ALS-mutant proteins: SOD1, FUS, TDP-43, and optineurin, providing an intriguing mechanism explaining Golgi fragmentation in patient tissues (Sundaramoorthy et al., 2013, 2015; Atkin et al., 2014; Soo et al., 2015a). Here, SOD1 is linked to amyotrophic lateral sclerosis.