This strategy was used by Stella and co-workers [57] during the evaluation of changes in both the cellular proteome and the secreted metabolome of primary spinal cord astrocytes derived from a widely used ALS mouse model, which overexpresses the human mutated (h)SOD1(G93A) protein, compared to (h)SOD1(WT) mice. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.