Surprisingly, despite being intrinsically disordered, TDP-43 PLD hosts almost all ALS-causing mutations and drives liquid–liquid phase separation (LLPS) of TDP-43, which is essential for functionally forming stress granules (SGs) composed of protein and RNA components but can also exaggerate into pathological aggregation or amyloid fibrils17. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.