The data presented in this paper demonstrating that TDP-43, FUS and SOD1 can form structurally distinct aggregates in the cell combined with the fact that TDP-43 and FUS have very different functions to that of SOD1 but result in the same disease phenotype is consistent with a unified model of toxic gain of function ALS protein aggregates. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.