When unopposed by pro-resolving mediators, the inflammatory response can propagate unimpeded and promote atherosclerotic plaque development in the arterial wall.118 Carotid endarterectomy analysis found an inverse relationship between the ratio of resolvin D1-to-LTB4 in the plaque and indices of vulnerability.119 Similar trends were observed in experimental atherosclerosis using LDL receptor-deficient mice (Ldlr−/−), and treatment with resolvin D1 significantly improved plaque stability. This evidence concerns the gene LDLR and atherosclerosis.