The amyloid cascade hypothesis suggested that accumulation of Aβ plaques is the primary cause of tau NFT formation69; however, it has also been suggested that the aggregation of toxic form of Aβ and tau might be independent processes separately contributing to the development of Alzheimer’s disease pathology.70 In addition, autopsy data have shown that the regional patterns of Aβ differ from that of tau deposition.71 Meanwhile, hypometabolism and atrophy are more closely related to tau accumulation as a downstream consequence of neuronal loss due to tau NFTs. The gene discussed is MAPT; the disease is Alzheimer disease.