Myocardial infarction (MI), following the occlusion of an atherosclerotic coronary artery, causes death of the cardiomyocytes and initiation of an inflammatory reaction, activation of the nuclear factor (NF)-κB and toll-like receptor (TLR)-mediated pathways, up-regulation of chemokines, cytokines as well as adhesion molecules in endothelial cells and leucocytes [1]. The gene discussed is NFKB1; the disease is myocardial infarction.