Previous research has shown that the Tg(SOD1*G93A)1Gur/J mouse model, which harbors the G93A mutation of the SOD1 protein (Wintz et al. 2023), is an important tool for studying ALS because it exhibits neuropathological changes similar to those seen in human ALS and is widely used to understand the mechanisms by which SOD1 mutations contribute to increased OS and apoptosis (Mazala et al. 2024). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.