Despite the challenges inherent to imaging tau pathology, which include its intracellular location; the presence of multiple human tau isoforms (three repeat [3R], four repeat [4R]) and morphologies (paired helical filament [PHF], straight filament [SF]); numerous post‐translational modifications (e.g., phosphorylation, truncation, nitration); and, in the case of Alzheimer's disease (AD), lower concentrations than amyloid beta (Αβ) in colocalizing tau and Aβ deposits (for review see Villemagne et al.2 The gene discussed is PPIB; the disease is Alzheimer disease.