In this scenario, exceeding this phase separation “threshold” – due to a mutation in an aggregate-prone RNA-binding protein, malfunction of signalling molecules and/or RNP granule disassembly factors – would cause abnormal stabilisation of RNP granules, with their subsequent persistence and associated toxicity, as seen in ALS/FTD (Fig. 1C, pathology 1). This evidence concerns the gene RNPC3 and frontotemporal dementia.