Methodological advancements support this aim, but do not overcome general shortcomings of DAT imaging to measure PD progression and severity, e.g. the flooring effect of DAT availability at advanced disease stages, or the involvement of several brain regions and neurotransmitter systems to PD pathology.39 Likewise, possible subtle effects of dopaminergic treatment on DAT binding cannot be excluded,40, –42 particularly in longitudinal evaluations as in our cohort, in which the levodopa equivalent daily dose increased from 238 ± 204 at baseline to 596 ± 391 at follow-up. The gene discussed is SLC6A3; the disease is Parkinson disease.