Although this study found that Nec-1 may improve myocardial cell oxidative stress and mitochondrial function by downregulating PARP1 expression and inhibiting AIFM1 nuclear translocation, ultimately alleviating heart failure in rats, previous research has also demonstrated that RIPK1 can interact with PARP1 to suppress oxidative stress or necrosis [36, 37]. The gene discussed is AIFM1; the disease is heart failure.