The autosomal nature of most (∼98%) of the ∼180 ALS-SOD1 mutations (2, 3, 4, 5) and the homodimeric nature of the SOD1 protein results in an early and ominous protein–protein interaction: heterodimerization of mutant and WT SOD1 (2, 6, 7, 8). Here, SOD1 is linked to amyotrophic lateral sclerosis.