Our study addressed two aims: (i) To take the influence of dopaminergic treatment on blood-based metabolomics into account, hypothesizing that this medication has a substantial impact on metabolomics in patients with IPD and monogenic PD and (ii) to identify dopaminergic medication–independent metabolites with different intensities in idiopathic and PRKN/PINK1-linked PD compared to HC by large-scale targeted metabolomics, hypothesizing that distinct alterations in metabolites might be characteristic for (“mitochondrial”) PD. The gene discussed is PRKN; the disease is Parkinson disease.