In recent research criteria, low Aβ42 or Aβ42/40 ratio and increased concentration of p-tau have been proposed to support the diagnosis of AD,1 with the AT(N) system classifying CSF Aβ and p-tau in the “A” and “T” categories, respectively.2 A proposed model of AD pathogenesis suggests that biomarkers reflecting Aβ pathology become abnormal before measures of tau pathology, which is now supported by a vast body of evidence.3 This evidence concerns the gene MAPT and Alzheimer disease.