Altogether, this result of the enhanced tau phosphorylation on tau residues Thr231, Ser396, and Ser404, confirms early to middle-advance tau PTMs probably associated to the initial steps to develop AD pathology, from the pre-NFT to the beginning of intracellular NFTs generation, since our cell model corresponds to fibroblast cells from FAD patients at a pre-symptomatic step (according to the data available at the Coriell Institute), and this could explain the absence of late-state markers of AD pathology in these cells. This evidence concerns the gene MAPT and Alzheimer disease.