In contrast, mice having AD‐causing human mutations knocked into the endogenous mouse APP locus bearing a humanized Aβ region (i.e., where the divergent moue Aβ residues [5, 10, and 13] have been changed to their human counterparts) accumulate high levels of human Aβ42 without changes in the expression of APP and its other constitutive fragments.5 The gene discussed is APP; the disease is Alzheimer disease.