A wide body of literature supports the negative impact and key role played by this phenomenon in the pathogenesis of AD [61], preceding the appearance of the two hallmarks of this disease represented by the abnormal deposition of Aβ (senile plaques) and the intracellular accumulation of hyperphosphorylated tau protein (neurofibrillary tangles) [62]. The gene discussed is MAPT; the disease is Alzheimer disease.