Mounting evidence indicates that galectin-3 is highly expressed and secreted by macrophages and drives alternative macrophage activation in myocardial repair after myocardial infarction [49], activates a variety of profibrotic factors, promotes fibroblast proliferation and transformation, mediates collagen production, and exhibits profibrogenic functions in chronic diseases [50]. This evidence concerns the gene LGALS3 and myocardial infarction.