Inhibition of RIPK1 inhibited programmed necrosis after myocardial ischemia-reperfusion, reduced myocardial infarction size, reduced inflammatory response, reduced the production of ROS, and then improved the function of cardiac remodeling in the infarcted area (Oerlemans et al., 2012). The gene discussed is RIPK1; the disease is myocardial infarction.