The Alzheimer’s disease clinical trial was halted because the participants developed aseptic meningoencephalitis due to an autoimmune response.[4], [8]–[10] Because amyloid beta-induced T-cell activation was considered responsible for the adverse event, we examined whether Ang II had the ability to trigger a T-cell-mediated immune response using T cell proliferation and ELISPOT assays. This evidence concerns the gene AGT and Alzheimer disease.