In addition, previous studies in ALS patients have demonstrated that cell death triggered by lipid peroxides (iron-dependent regulated necrosis) resulted in significant downregulation of endogenous mechanisms involved in protecting cells against ferroptosis, such as the glutathione peroxidase 4 anti-oxidant defense checkpoint (GSH/GPX4), and has been associated with degeneration of MNs and disease progression in ALS (sALS and fALS), suggesting a potential link between ALS and ferroptosis [11,16,25]. Here, GPX4 is linked to amyotrophic lateral sclerosis.