The authors suggested the activation of the RIP1/RIP3/MLKL necroptotic pathway as responsible for the differences observed in both groups, as treatment of KO mice with necrostatin-1s, a RIP1 kinase activity suppressor and necroptosis inhibitor, decreased the infarction size and myocardial dysfunction after ischemia/reperfusion injury (Qin et al., 2016). The gene discussed is MLKL; the disease is infarction.