By up-regulating apoptotic signals and the phosphorylation of mitogen-activated protein kinase (MAPK) signaling pathways, the overexpression of FABP3 has been shown to promote myocardial cell death in a myocardial infarction mouse model, whereas deficiency in FABP3 can effectively prevent ischemic heart injury [79]. This evidence concerns the gene FABP3 and myocardial infarction.