As Wang et al. (68) have conducted in vivo and in vitro experiments by using respectively ApoE mice fed with high-fat diet (HFD) and THP-1 macrophages, and they have demonstrated that Mel can promote autophagy and inhibit atherosclerotic inflammation by down-regulating Gal-3, which means that Mel is expected to be a therapeutic strategy for atherosclerosis. Here, LGALS3 is linked to atherosclerosis.