The beneficial effects of EPA in cardiovascular prevention, together with the potent proresolving and anti-atherosclerotic actions mediated by the EPA-derived lipid mediator RvE1 through its receptor ChemR23, put the spotlight on the potential therapeutic benefits of stimulating the EPA/RvE1/ChemR23 pathway to promote resolution of atherosclerotic inflammation and to improve the outcomes of atherosclerosis-related cardiovascular disease. This evidence concerns the gene CMKLR1 and atherosclerosis.