Conversely, several proteins showed reduced association with UBQLN24XALS, including FAM168A/TCRP1, implicated in Polβ stabilization and base excision repair (Liu et al., 2015) and BAX, a pro-apoptotic factor involved in mitochondrial stress responses (Walensky and Gavathiotis, 2011) that was deenriched in UBQLN2P497H and UBQLN24XALS IPs relative to wild-type, suggesting potential LOF interactions shared across ALS alleles. This evidence concerns the gene FAM168A and amyotrophic lateral sclerosis.