Researchers at The Jackson Laboratory, the Broad Institute and Yale mapped the regulatory activity of more than 220,000 single‑nucleotide variants across five human cell types using a massively parallel reporter assay, resolving causal noncoding variants within loci linked to complex traits. The work identified functional variants that modulate gene expression and clarified mechanisms underlying associations for traits such as blood pressure, lipids and glycemic control. The high‑throughput dissection converted large GWAS loci into testable biological hypotheses, allowing geneticists and drug developers to prioritize variants and target genes for therapeutic follow‑up. The study’s single‑nucleotide resolution accelerates the translation from association to mechanism, facilitating better target selection and potential biomarker discovery. For translational genetics and precision medicine, these maps reduce ambiguity in causal inference and can guide target de‑risking efforts that inform preclinical modeling, target validation, and clinical trial design.