Background For many complex diseases, including Parkinson’s disease, regulatory elements located in intergenic regions have been putatively associated with disease risk and development. However, the biological mechanisms linking these intergenic loci to disease pathogenesis remain largely unknown. Fundamentally, this is because these intergenic loci are non-coding, and bespoke approaches to in-depth functional characterisation are required. Here we utilised an integrative, functional approach to identify the genotype-specific impacts of Parkinson’s disease-associated variant rs11610045, located within a complex region on chromosome 12. Methods & Results We utilised CRISPR-Cas9 editing (and reversal) to generate isogenic iPSC clones from the KOLF2.1J line containing either the A|A (WT) or G|G (edited) rs11610045 genotype. We also reverted the G|G genotype back to the A|A genotype in two clones to control for off-target effects. Functional profiling of these clones demonstrated allele-specific regulation of both nearby and distal genes, including THBS1 and PDGFB. Further, affinity purification followed by mass spectrometry identified the differential binding of potential regulatory proteins to the G|G genotype compared to the WT A|A genotype, including the transcription factor TCF7L1. Conclusions Our findings support a model in which non-coding variants, such as rs11610045, impact the expression and downstream activity of multiple genes predominantly through trans-acting mechanisms. In so doing, this study demonstrates a pipeline to delineate SNP-specific impacts in an iPSC model. Finally, we highlight the challenge of aligning genotype dependent expectations of the impact of expression quantitative loci on genes as part of the exploration of how inherited genetic variation contributes to complex genetic disease.