The tight coupling between CSF phosphorylated tau measures, particularly pT217/T217, pT111/T111, pT213/T231 and pT153/T153, and traditional amyloid markers across the disease spectrum supports the changing view in the field that these markers reflect a response to amyloidosis rather than a soluble measure of NFT pathology as measured by tau PET.1,10,14,56 Similar results have been seen with other older adult cohorts11,12 as well as autosomal dominant Alzheimer’s disease.57 The gene discussed is MAPT; the disease is amyloidosis.