In vivo studies in mice have shown that the disease-related gene mutations in FUS alter the properties of proteins, leading to the abnormal phase transition and loss and toxic gain of function, and induce the conformational changes in the related proteins, resulting in one of the pathological markers of ALS, which is the magnocellular-like aggregation, and the further consolidation and growth of fibrous structures (Korobeynikov et al., 2022). Here, FUS is linked to amyotrophic lateral sclerosis.