In this study, they proved that the inhibition of the NF-κB signaling pathway can improve cardiac function after MI and prognosis since NF-κB can regulate many proinflammatory cytokine transcriptions such as TNFα, IL-6, and monocyte chemotactic protein (MCP-1), which not only cause myocardial cell hypertrophy and apoptosis but also affect the myocardial systolic function leading to ventricular remodeling occurrence and heart failure [77–79]. The gene discussed is NFKB1; the disease is myocardial infarction.