To date, most experimental therapeutics have focused on modulation of the major pathologic features of the AD brain by designing drugs that decrease formation of the 42-amino acid amyloid beta peptide (Aβ1–42) or modify its capacity for formation of neurotoxic oligomers or the modulation of tau hyperphosphorylation and NFT formation through manipulation of kinases responsible for tau phosphorylation. The gene discussed is MAPT; the disease is Alzheimer disease.