Our lab uses human genetics to identify new mechanisms driving coronary artery disease (CAD). Starting with findings from genome-wide association studies (GWAS) of CAD, we identify the causal gene at a given locus, study the effect of this gene on cellular and vessel wall biology, and finally determine the molecular pathways by which this gene influences CAD risk. Within this framework, we use complex genetic mouse models and human vascular samples, single-cell transcriptomics/epigenomics and high-throughput CRISPR perturbations, as well as traditional molecular biology techniques.