In an animal model study concerning myocardial infarction (MI), Zhang et al. revealed that knockdown of Rap1 resulted in downregulation of NF-κB activity characterized by reduced proinflammatory paracrine cytokines (TNF-α, IL-6, and monocyte chemotactic protein-1) and increased the resistance to hypoxia-induced apoptosis in MSCs. The gene discussed is CCL2; the disease is myocardial infarction.