Recently, a next-generation AD mouse model was presented, which circumvented the aforementioned confounders by a knock-in strategy that introduced Swedish (K670N/L671M) and Iberian/Beyreuther (I716F) mutations into the endogenous mouse APP gene, whose Aβ sequence was ‘humanized’ by the exchange of three codons within the Aβ coding sequence [12]. This evidence concerns the gene APP and Alzheimer disease.