Interestingly disruption of ER/mitochondria contacts appears to be a common phenomenon in ALS with reduced ER/mitochondria contact sites found in mutant SOD1, Sig1R, TDP-43, and FUS-related ALS (Lautenschlager et al., 2013; Stoica et al., 2014, 2016; Watanabe et al., 2016). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.