A previous study indicated that the ideal therapy for MI‐induced cardiac injury was to inhibit the reactive fibrosis (and other remodelling processes) as well as the regeneration of the infarct area in non‐infarcted areas.32 Tanshinone IIA suppresses cardiac fibrosis by regulating the paracrine factors released by cardiomyocytes that go on to activate the TGF‐b/Smads signalling pathway.9 Tan IIA could also mitigate BLM‐induced pulmonary fibrosis and suppress the TGF‐β‐dependent mesenchymal transition (EMT) in lung alveolar epithelial cells.33 Here, TGFB1 is linked to myocardial infarction.