Consistent with this notion, in AD pathology, the accumulation of amyloid plaques (APs), constituted of amyloid-beta peptide (Ab) aggregates, and neurofibrillary tangles (NFTs), constituted of misfolded Tau proteins, is related to a deficiency in the activation of cytoprotective proteins (Hsps) or, more generally, of cellular stress tolerance pathways [55]. The gene discussed is MAPT; the disease is Alzheimer disease.