The leading hypothesis for the development of tau pathology in Alzheimer’s disease is that it is a downstream event of amyloid beta (Aβ) plaque pathology, and that abnormal phosphorylation of tau causes the protein to detach from the microtubules, thereby destabilizing them, leading to axonal degeneration and the aberrant aggregation of tau into paired helical filaments, which in turn assemble into neurofibrillary tangles [3]. The gene discussed is MAPT; the disease is Alzheimer disease.