In addition, the up-regulation of gal-3 in the process of heart disease results in macrophage migration and fibroblast proliferation, which leads to fibrosis (de Boer et al., 2009), which has also been confirmed by vergaro who thought galectin-3 may be related to myocardial fibrosis in NICM patients evaluated by LGE (Vergaro et al., 2015), but this result still needs a large number of samples to further verify. This evidence concerns the gene LGALS3 and heart disorder.