This hypothesis was confirmed by over‐expressing 3R human tau driven by the tubulin‐α1 promoter in the tau ko mice generated by Dawson and colleagues, shifting the accumulation of abnormal tau aggregates into astrocytes and oligodendrocytes, but not neurons, together with a loss of both glial cells and neurons and progressive motor disturbances such as weakness and dystonia (Higuchi et al. The gene discussed is MAPT; the disease is Dystonia.