If seeding of WT SOD1 by TDP-43 occurs in sporadic ALS, manifesting neurotoxicity in addition to TDP-43 toxicity mediated by nuclear depletion and cytoplasmic aggregation and then inhibiting the intermolecular interactions between TDP-43 and SOD1 may represent a target for interventions to slow disease progression. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.