This remodeling involves both aberrant gains of interaction with stress-responsive proteins (e.g., PEG10, BAG6, HYOU1) and loss of interactions (e.g., VKORC1L1, BAX), pointing to a complex interplay of gain- and loss-of-function mechanisms in UBQLN2-linked ALS. This evidence concerns the gene BAX and amyotrophic lateral sclerosis.