Multiple studies have shown an association between KTN1 variants and changes in expression levels and brain structure including frontal cortex, putamen (Hibar et al., 2015), nucleus accumbens, caudate nucleus, and globus pallidus regions (Satizabal et al., 2019). Recently, Mao and colleagues reported nominal associations between common intergenic variants up- and downstream of the KTN1 gene and PD risk (Mao et al., 2020). They also noted increased KTN1 mRNA expression in the putamen and substantia nigra pars compacta (SNpc), which resulted in a compensatory increase in the gray matter volumes (GMV) of these two brain regions in PD patients, suggesting that KTN1 may play a functional role in the development of PD (Mao et al., 2020). As part of the International Parkinson’s Disease Genomics Consortium (IPDGC) efforts to investigate and replicate reported PD risk factors, we sought to assess the role of KTN1 as a genetic risk factor for PD within large European cohorts. We considered KTN1 variants to account for their potential role in regulating KTN1 mRNA expression in the putamen and SNpc.