Similar to sporadic AD, the decrease in CSF Aβ42 is followed later by increased 11 C Pittsburgh compound-B (PiB) binding in positron emission tomography (PET) and evidence of tau pathology and neurodegeneration [9, 12], aligning with the order of the A/T/N classification concept [13] and the amyloid cascade hypothesis [1]. The gene discussed is MAPT; the disease is Alzheimer disease.