Although Aβ peptides, especially Aβ(1–42), are known to play an active role in the development of AD [1], recent observations suggest that extracellular Aβ fibrils and plaques are relatively inert [2], like other amyloid fibrils (e.g. those formed by Islet Amyloid Polypeptide, IAPP [3]), raising questions about the precise mechanism of Aβ peptides. Here, IAPP is linked to Alzheimer disease.