Our goal is to identify and validate causal pathways in cardiovascular disease. Large-scale genome-wide association studies (GWAS) have been very fruitful in pinpointing genomic regions that associate with the disease. However, the precise mechanisms underlying most of these genetic associations remain elusive. To this end, we use both computational and experimental approaches to expose new mechanisms leading to atherosclerosis, the major cause of cardiovascular disease. We apply cutting-edge technology, including human induced pluripotent stem cells and CRISPR/Cas9 genome editing, to elucidate the biological underpinnings of candidate causal genes and pathways. In parallel, we conduct recall-by-genotype studies, in which individuals with a functional genetic variant are called back for additional hypothesis-driven phenotyping. Our efforts, which integrate genetic epidemiology, functional genomics/epigenomics, and clinical medicine, facilitate a better understanding of the aetiology of cardiovascular disease to inform the development of new therapeutics.