In AD subjects, there is an overproduction of Aβ peptides that would depend on several events acting more or less in parallel, i.e., an increase of APP expression and the amyloidogenic APP processing [6, 7], reduction of the protective APP cleavage by α-secretases [8, 9], and/or impairment of Aβ-degrading enzymes [10]. The gene discussed is APP; the disease is Alzheimer disease.