We suggested earlier that the development of selective 4R tracers could facilitate the differentiation of 4R-tauopathies not only from healthy controls but also from AD cases with predominant presence of 3/4R tau.31 Despite the different magnitude and spatial extent of brain tau deposition, [18F]PI-2620 binding properties were already able to differentiate 3/4R from 4R tauopathies. The gene discussed is MAPT; the disease is tauopathy.