Excessive phosphorylation of tau at the threonine 231 residue (Thr231) lowers the ability of tau to bind to microtubules, and may lead to neuronal cytoskeleton disruption; this modification is associated with p-tau pathological aggregation in the cell and is identified in NFTs in AD brains [7,8,9,10,11] In line with this, phosphorylation at Thr231 has been shown to be one of the consistently increased post-translational modifications of tau in the brain that distinguishes neuropathological Braak stages 0–I from III–IV [12,13]. The gene discussed is MAPT; the disease is Alzheimer disease.