This added clarity around the mechanism by which OGA inhibition reduces tauopathy, the demonstration that nearly complete inhibition of OGA is required to achieve a measurable pharmacodynamic effect (increase in O-protein), the development of sensitive high throughput assays for detection of this pharmacodynamic effect and the identification of CSF total tau as a potential translational biomarker will support the clinical development of OGA inhibitors. The gene discussed is OGA; the disease is tauopathy.