Next, we obtained datasets from animal models with a genetic risk of a neurodegenerative disease: mice with transgenic expression of a G93A mutant form of human SOD1, as a model of ALS (#1: GSE46298, #2: GSE18597)55,56; transgenic mice with mutant human amyloid precursor protein (APP) and presenilin1 (PSEN1) genes, which cause familial Alzheimer’s disease (#1: GSE64398, #2: GSE64398)57; and Df16(A) heterozygous mice carrying a chromosome 16 deletion syntenic to human 22q11.2 microdeletions, as a model of schizophrenia (GSE29767)58. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.