Since the tau MTBR forms the core of the neurofibrillary aggregates characteristic of tauopathies and is the site of most exonic mutations that drive familial tauopathies [6, 19, 20], the modulation of tau:MT and tau:tau interactions via tau phosphorylation [1, 3, 13, 21] or cleavage [22–25] to form toxic oligomers or aggregates [26] has become the central research focus in studies of tau-induced toxicity and tauopathy cytopathogenesis. Here, MAPT is linked to tauopathy.