In animal experiments, overexpression of S100A1 improved the cardiac function of IHF animal models, whereas a lack of S100A1 led to increased arterial pressure and mortality after myocardial infarction in mice (Jungi et al., 2018; Pleger et al., 2011; Soltani et al., 2021). The gene discussed is S100A1; the disease is myocardial infarction.