In summary, genetic alterations favoring LOXIN isoform production coupled to the observation that this isoform exerts a dominant-negative effect on LOX-1 function make it an attractive new target for prevention and treatment of initiation, progression, and clinical consequences of atherosclerosis such as plaque instability, acute myocardial infarction, and ischemia reperfusion injury. This evidence concerns the gene OLR1 and myocardial infarction.