In their study, M.I. Oerlemans et al. demonstrated that RIPK1, RIPK3, and mixed lineage kinase domain-like (MLKL) expression was up-regulated in the myocardium after reperfusion, and the necrosis inhibitor Necrostatin-1 could reduce the phosphorylation levels of RIPK1 and RIPK3 and the recruitment of MLKL, thus inhibiting cell necrosis and reducing myocardial infarct size (Oerlemans et al., 2012). This evidence concerns the gene MLKL and myocardial infarction.