The vast majority of mutations in FUS/TLS-related familial ALS cases were identified in C-terminal NLS, which result in the retention and the inclusion of FUS/TLS in the cytoplasm [2], [3], [5], [8], [14], and FUS/TLS as well as TDP-43 is recruited to SGs under stress conditions such as arsenite, heat shock and hypoxia [28], [29], [30]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.