Most drugs tested for AD in the past 20 years have targeted the accumulation of the Aβ with a focus on decreasing levels of Aβ monomers, oligomers, aggregates, and plaques using compounds that decrease production, antagonize aggregation, or increase brain clearance of Aβ, such as β-site amyloid precursor protein cleaving enzyme 1 (BACE-1) inhibitors, and anti-Aβ antibodies [64,65,66]. The gene discussed is BACE1; the disease is Alzheimer disease.