Further evidence revealed that circFndc3b was down-regulated in cardiomyocytes, and restoration of its expression promoted cardiac function and remodeling after MI through inhibiting cardiomyocyte apoptosis and evoking neovascularization via FUS/VEGF-A axis (Garikipati et al., 2019[11]). The gene discussed is VEGFA; the disease is myocardial infarction.