Given that TG models reliant on APP overexpression exhibit elevated levels of APP and its metabolites, it is reasonable to infer that in these models, cognitive deficits and other abnormalities could predominantly stem from increased expression of APP, soluble APP ectodomains, and/or APP C‐terminal fragments, rather than being primarily driven by Aβ oligomers and amyloid pathology. The gene discussed is APP; the disease is amyloidosis.