The fact that AD‐causing mutations in APP and in presenilins 1 and 2 alter APP proteolytic processing in a way that elevates the relative levels of the Aβ42 or Aβ43 peptides has long been known (Scheuner et al, 1996; NB: Those mutations in APP that lie within the Aβ sequence increase the self‐aggregation of the resultant peptides, not their production). The gene discussed is APP; the disease is Alzheimer disease.