This SOD1 toxic gain-of-function is believed to induce neuronal cell death through mechanisms such as excitotoxicity, calcium overload, oxidative stress, and mitochondrial dysfunction, ultimately contributing to the onset and progression of ALS (Hayashi et al., 2016; Kawamata and Manfredi, 2010; Peggion et al., 2022). Here, SOD1 is linked to amyotrophic lateral sclerosis.