Although tau is intrinsically disordered, under normal conditions, it stabilizes microtubules in neurons; however, in AD and other tauopathies, tau undergoes several post translational modifications, including abnormal phosphorylation, oxidation, conformational changes, and truncation, all which have been reported to contribute to its aggregation into paired helical filaments (PHFs), which make up neurofibrillary tangles (NFTs) [1, 2]. The gene discussed is MAPT; the disease is Alzheimer disease.