Given the significant extension of lifespan in SOD/OXR1 mice, we next determined neuroprotective effects of OXR1 overexpression by comparing behaviour and pathology of SOD/+ mice to that of SOD/OXR1 mice at the same time-points during ALS disease pathogenesis, a method commonly used in studies examining genetic modifiers of SOD1-mediated ALS (Boillee et al., 2006; Yamanaka et al., 2008; Hetz et al., 2009; Van Hoecke et al., 2012; Frakes et al., 2014; Seijffers et al., 2014). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.