The identified mechanism, together with the finding that miR‐486‐mediated SRSF3 silencing simultaneously decreases the expression of fibrosis effector genes (PAI‐1, TSP‐1 and α‐SMA), which are well‐established important activators of fibrotic activity,3, 22, 23, 24, 25, 26 improves cardiac fibrosis and post‐MI remodelling, thereby providing beneficial effects to enhance MI regeneration. The gene discussed is THBS1; the disease is myocardial infarction.