AD’s neuropathology leans on a triad of hallmarks: (i) extracellular congophilic plaques of insoluble fibrillar amyloid-β peptides (fAβs); (ii) intracellular insoluble aggregates (neurofibrillary tangles or NFTs) of hyperphosphorylated Tau proteins (p-Taues); and (iii) a diffuse chronic neuroinflammation [3,4]. The gene discussed is MAPT; the disease is Alzheimer disease.