Indeed, S100A1 knock-out mice showed enhanced susceptibility to functional deterioration in response to chronic cardiac pressure overload stress and ischemic damage.27,28 In contrast, mice with overexpression of S100A1 are hypercontractile and maintained almost normal left ventricular function following myocardial infarction.28 Studies in a large-animal model of heart failure suggested that S100A1 may be an attractive target of cardiac gene therapy.29 This evidence concerns the gene S100A1 and myocardial infarction.