By filter retardation assay, we have recently determined that protein aggregates of TPC6A and TIAF1 are present in the hippocampus of normal middle-aged individuals, and the TPC6A/TIAF1 complexes possess increasing amounts of Aβ in AD patients.1 The aggregated TPC6AΔ induces TIAF1 aggregation and activates caspases for causing APP degradation and Aβ generation. The gene discussed is APP; the disease is Alzheimer disease.