Familial ALS-associated SOD1 mutants (A4V and G93A)13,15 were efficiently recruited in hypoxia/acidosis- and heat shock-induced A-bodies (Fig. 2D,E), whereas none of the disease-associated FUS (F521H and P525L), TDP-43 (A315T and M337V), or TIA1 (P362L and A381T) mutations altered the affinity of these proteins for this subnuclear domain (Fig. 2A–C,E). Here, FUS is linked to amyotrophic lateral sclerosis.