Experimental loss-of-function studies in mice, mainly on TLR2 and TLR4, demonstrated that inhibition of TLR2 was beneficial in the pathology of atherosclerosis and ischemia/reperfusion injury after myocardial infarction, similar to the finding that long-term administration of TLR2 agonists significantly increased experimental atherosclerosis (79–82). The gene discussed is TLR4; the disease is atherosclerosis.