RIPK3 and myocardial infarction: 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).