Inhibition of MPO improved the motor performance of SOD1G93A transgenic mice.[242] The activation of MPO/HOCl pathways facilitated ferroptosis through inhibiting the expressions of GPX4 and NQO1 and thus leading to irreversible lipid peroxidation.[242] These results suggested that aggregation of mutant hSOD1 proteins led to activation of the MPO/HOCl pathway, triggering ferroptosis in ALS.[242] Overexpressed FSP1 could ameliorate ferroptosis in SOD1G93A ALS NSC‐34 motor neurons models, evidenced by suppressed the MDA levels. This evidence concerns the gene MPO and amyotrophic lateral sclerosis.