However, at the least, our data clearly demonstrated that HMGB1 was a direct risk factor of cardiac fibrosis; some reports were not consistent with our data; their data showed that exogenous HMGB1 could attenuates cardiac remodelling, and improves cardiac function after myocardial infarction (MI) by inducing myocardial regeneration [44,45]. Here, HMGB1 is linked to myocardial infarction.