To test the functional significance of this increased insolubility of FUS and other RBPs, we looked in the mutant animals for evidence of aberrant splicing of their target pre-mRNAs, similar to that which we described previously in brain and spinal cord tissue from C9orf72-positive and gene-negative patients with ALS/FTD27. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.