GPX3 forms a protein–protein interaction with another antioxidant enzyme, SOD1 (superoxide dismutase) [67], encoded by the first-discovered ALS risk gene [68]; GPX3 is downregulated in both ALS patients and ALS mouse models [69, 70]; and knockdown of gpx3, but not tnip1, caused motor defects in zebrafish [70]. Here, TNIP1 is linked to amyotrophic lateral sclerosis.