LDLR and myocardial infarction: The clinical data are supported by ex vivo experimental evidence, where administration of HDL provides protection against ischemia–reperfusion injury in rodent hearts [4,5], and in vivo experimental evidence demonstrates that overexpression of apolipoprotein (apo) A1 (the major protein component of HDL) protects low-density lipoprotein (LDL) receptor (LDLR−/−) knockout mice from coronary artery ligation-induced myocardial infarction, cardiac dysfunction, and death [6].