Mounting evidence has shown that accumulation of aggregates of amyloidgenic proteins, such as Aβ and tau in AD and α-synuclein (αS) in PD, may be central to the pathogenesis of neurodegenerative diseases.1,2 According to the notion that neurotoxicity may be attributed to the aggregates of amyloidogenic proteins, particularly oligomers and protofibrils.5 Thus, it is reasonable to predict that suppressing expression of amyloidogenic proteins and/or inhibiting protein aggregation may be effective to delay the progression of neurodegenerative disease. The gene discussed is MAPT; the disease is neurodegenerative disease.