Additionally, SOD1-ALS pathway molecules, such as ACTB, PFN1, SLC1A2, CASP1, and TP53 also play a part in the development of SOD1-provoked ALS (Figure S2), while FAS, PTGS2, PARK7, IL1B, IL6, APP, and CALM1 (calmodulin 1) engage in SOD1-triggered neurodegeneration in ALS (Figure S3). This evidence concerns the gene PARK7 and amyotrophic lateral sclerosis.