Although most mouse models expressing human β-amyloid fail to induce NFTs comprising mouse tau within the murine lifespan [104–106], the presence of Aβ oligomers or APP with fAD mutation(s) is invariably associated with increased tau pathology in tau transgenic mice [107, 108], tauopathy models in rats [109], non-human primates [110], and in 3D human iPSC (induced pluripotent stem cell)-derived neuronal cell culture systems [111–114]. The gene discussed is MAPT; the disease is tauopathy.