Although substantial differences in aggregation profiles of SOD1, TDP-43 and p62 in SOD1-fALS, non-SOD1-fALS and sALS cases imply distinct pathways drive neurodegeneration in each ALS subgroup [11], the presence of common pathologies across subgroups indicates some pathways may be common to all patients, irrespective of the presence or absence of key gene mutations. Here, SOD1 is linked to amyotrophic lateral sclerosis.