SOD1 and amyotrophic lateral sclerosis: Tsioras and colleagues (2023) [212] demonstrated that the accumulation of insoluble mutant SOD1 protein in an ALS-hiPSC-derived MN model interfered with the turnover of a series of proteins mainly involved in protein folding and cytoskeletal homeostasis; the valosin-containing protein (VCP), which plays a key role in ubiquitin-based degradation, accumulated with mutant SOD1 and modified its interactome, most likely affecting its role to maintain cellular homeostasis through the clearance of misfolded proteins, such as mutant SOD1.