For example, humanized App KI rats carrying either the pathogenic APP Swedish mutation or the PSEN1 mutation (PSEN1L435F) do not form plaques, whereas rats harboring both mutations exhibit amyloid plaques that replicate the distribution, characteristics, and Aβ‐species composition amyloid plaques observed in AD patients (Tambini et al, 2023). This evidence concerns the gene PSEN1 and amyloidosis.