Moreover, Winter et al. [123] concluded that elevated levels of circulating GAL-3 were strongly associated with premature myocardial infarction and that GAL-3 might serve as a link between dyslipidemia (as a driving force of plaque formation) and inflammation (as an initiator of plaque rupture) in patients with premature acute myocardial infarction. This evidence concerns the gene LGALS3 and acute myocardial infarction.