Several experimental models displayed the interaction of Reelin with deposits of amyloid precursor (APP) and beta-amyloid (Aβ), hyperphosphorylated TAU protein, linkage with the disequilibrium between T-helper and T-reg lymphocytes and finally the indirect association with cellular ferroptosis, hallmarks of neurodegenerative disorders, including AD [5,6,7,8]. This evidence concerns the gene RELN and Alzheimer disease.