After observing the likely involvement of ATF3 in SOD1-mutant ALS pathogenesis observed in PBMCs and the potential centrality of SNAP25 within the network of genes localized to transcriptionally silenced H3K27me3-marked chromatin unique to the SOD1 sample group, we investigated first in a bioinformatics framework then experimentally whether SNAP25 is among the target genes ATF3 acts on. Here, SNAP25 is linked to amyotrophic lateral sclerosis.