Future research should focus on recruiting far larger cohorts, preferably hundreds of subjects, including tau deposit measurements to determine whether there are indeed specific general or individual thresholds of β‐amyloid build‐up that would precipitate cognitive decline or whether β‐amyloid accumulation genuinely functions as a protective mechanism that ultimately fails, allowing for the breakthrough of clinical symptoms seen in Alzheimer's disease. The gene discussed is MAPT; the disease is Alzheimer disease.