While in vivo studies have been critical for determining the cross-species seeding abilities of different pathological tau strains [132] and in demonstrating that pathological inclusions from human brains affected with tauopathies induce NFT formation in rodents, often recapitulating the disease-specific features of the original inclusion [113, 133, 134], the molecular mechanisms underlying tau propagation remain challenging to assess in vivo. The gene discussed is MAPT; the disease is tauopathy.