While a research framework for defining AD based on beta amyloid (Aβ) deposition, pathologic tau, and neurodegeneration (ATN) has been proposed (Jack et al, 2018), clinical criteria for AD are not universally standardized and range from clinical presentation to brain imaging by MRI and PET to clinical chemistry analysis of Aβ1–42/Aβ1–40, total‐tau (t‐tau), and phosphorylated‐tau (p‐tau181) in cerebrospinal fluid (CSF; Frisoni et al, 2010; McKhann et al, 2011; Ferreira et al, 2014; Rice & Bisdas, 2017). The gene discussed is MAPT; the disease is Alzheimer disease.