In vivo research did not specifically deplete Tregs or AREG+ Tregs in mice; instead, we used anti-CD25 antibody for non-specific Treg cell depletion or IL-2/JES6-1 complex to expand Tregs in vivo, or intravenously injected cultured Tregs and AREG-overexpressing Tregs to assess their impact on post-myocardial infarction cardiac function, fibrosis, and angiogenesis. Here, IL2 is linked to myocardial infarction.