This popular and well-accepted theory of amyloid-triggered tauopathy model has been sufficiently supported by numerous preclinical studies: in vivo studies on genetically-engineered murine models with Aβ-related gene insults reveal that toxic Aβ species stimulates the formation of pathological tau by altering the activities of the protein kinases and phosphatases that regulate tau phosphorylation as well as directly inducing tau misfolding, indicating that the two pathological hallmarks develop codependently [2, 3]. This evidence concerns the gene MAPT and tauopathy.