It also demonstrated that cytosolic mis-localization of FUS or TDP-43 in vitro and in vivo in ALS patients may kindle wtSOD1 misfolding in non-SOD1 fALS and sALS, and how indirect induction of SOD1 misfolding is possible, especially as the lack of immunohistochemical compartmental co-localization of said proteins still propagated SOD1 misfolding beyond its site of inception. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.