The recently identified APP variant Ala673Thr, which is less efficiently cleaved by BACE1 [32], together with studies on AD-transgenic mice crossed with genetically deleted BACE1 mice, showing a decrease in Aβ levels and protection against AD and cognitive decline [33, 34, 35, 36, 37], strongly suggest that BACE1-inhibition should prove effective for AD treatment. This evidence concerns the gene BACE1 and Alzheimer disease.