While most recent AD therapeutic development has focused on the removal of Aβ or prevention of its aggregation into plaques, the recent findings by Oddo et al and Santacruz et al. that tau accumulation can only be reversed at an early stage in its AD pathogenesis highlights the need for therapeutic strategies to slow or even stop tau accumulation in this disease and other hereditary tauopathies [5,7]. This evidence concerns the gene MAPT and Alzheimer disease.