The mechanism by which mutations in FUS, TARDBP (TDP-43) and other genes encoding RBPs cause neuronal degeneration in ALS remains unclear, but a compelling model of disease argues that toxicity involves the formation of abnormal assemblies or condensates of protein and RNA that arise as a consequence of a natural process of LLPS that is critical for the normal, reversible functions of these regulatory proteins. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.