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. The gene discussed is VKORC1L1; the disease is amyotrophic lateral sclerosis.