Despite being well-established that tau neurofibrillary tangles (NFT) and β-amyloid (Aβ) plaques are the hallmarks defining the neuropathology of this disease, it is not yet completely clear how much they contribute to neuronal degeneration spreading or if they may be just byproducts of ongoing damage [3]; this has been fully recognized and has led to the idea that other pathological processes can significantly contribute to AD pathogenesis as well [4]. The gene discussed is MAPT; the disease is Alzheimer disease.