The clinical benefit of confirming pathological DAT availability is negligible in patients with a clear metabolic pattern of PD (i.e. hypometabolism in the temporoparietooccipital cortex), MSA (i.e., hypometabolism in the posterior putamen and cerebellum), or PSP (i.e., hypometabolism in the medial and dorsolateral frontal cortex, caudate, and thalamus)5. The gene discussed is SLC6A3; the disease is supranuclear palsy, progressive, 1.