While condensation of TDP-43 and FUS via LLPS is indispensable for their physiological functions, aberrant phase transitions can convert dynamic condensates to gel- or solid-like assemblies, suggesting that dysregulated LLPS might play a role in the initiation of their pathological aggregation in neurodegenerative diseases [228–230] (Fig. 4A). This evidence concerns the gene TARDBP and neurodegenerative disease.