Our GSEA supports these observations, showing that reduced SLC30A3 correlates with enrichment in pathways linked to synaptic plasticity (LTP, LTD, calcium signaling, axon guidance), mitochondrial energy metabolism (TCA cycle, oxidative phosphorylation), and multiple neurodegenerative disorders (Parkinson’s disease, Huntington’s disease, ALS). This evidence concerns the gene SLC30A3 and amyotrophic lateral sclerosis.