ALS-linked mutations in SOD1 result of exposure of more hydrophobic surfaces in the mSOD1 proteins, which enhances the propensity for non-native interactions with itself and other proteins and subsequent self- and co-aggregation [53], [54], and this may be the underlying mechanism driving the increased interaction of COMMD1 with mSOD1. Here, COMMD1 is linked to amyotrophic lateral sclerosis.