The neuropathological signatures of AD are characterized by the presence of extracellular deposits of amyloid β (Aβ) and intracellular aggregates of hyperphosphorylated Tau proteins.[1] Currently, drugs targeting Aβ have two main limitations: their limited efficacy, which does not sufficiently alleviate the clinical symptoms of patients with AD, and their significant toxicity and side effects, making them unsuitable for extended use.[2] Thus, there is an urgent need to find a potent medication with low toxicity for daily administration to AD patients. Here, MAPT is linked to Alzheimer disease.