In some ALS and FTLD cases, however, the pathological SGs are colocalized with amyloidogenic deposits because the SG marker proteins TIA-1 and TDP-43 can form both SGs and insoluble fibrillary aggregates under pathological conditions and because SGs may function as seeds for irreversible aggregation (reviewed in [77]). This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.