FLT4 and myocardial infarction: Since the Harvard study in the 1980s,7 which was the first article about the cardiac lymphatics during fibrotic repair and regeneration after MI, many investigators observed that an increase in VEGF-C–VEGFR-3 signaling after myocardial infarction could significantly promote lymphangiogenesis, reduce myocardial edema, alleviate the degree of inflammation and fibrosis, and improve cardiac function in murine models.12,25,34 Our own data (as yet unpublished) also showed that increased ephrinB2 signaling enhances lymphangiogenesis after MI.