In the highest-dosage group, CSF SOD1 levels declined 36% with some evidence of a reduction in disease measures; however, a correlation between treatment and clinical outcomes could not be drawn due to the small study size.63 Therefore, the use of SOD1 as a biomarker may lie primarily in determining the pharmacodynamics of SOD1-lowering therapies as opposed to differentiating between subtypes of amyotrophic lateral sclerosis. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.