Already decades before onset of clinical symptoms of Alzheimer’s disease (AD), an imbalance between production and clearance of the amyloid-β (Aβ) protein leads to aggregation of the protein into soluble oligomers and protofibrils, eventually forming insoluble fibrils, which precipitate into the brain tissue as more or less densely packed plaques. The gene discussed is PROS1; the disease is Alzheimer disease.