Both App KI mouse strains showed relevant amyloid deposition composed of pathological Aβ42, similar to that in AD patients (Fig. 2).9 Advantages associated with using the App KI strains have been described,10, 11 with these mouse strains showing fewer artifactual anomalies compared with APP overexpressing mice.12, 13 However, we did not observe NFT in the App KI mice during their lifespan, suggesting that the mice might also be useful as preclinical AD mouse models to investigate the pathological role of amyloidosis and amyloid‐associated neuroinflammation. This evidence concerns the gene APP and Alzheimer disease.