Since the anti-inflammation action of IGFBP3 is possibly attributed to its potential of inhibiting nuclear factor-κB (NF-κB) [57], further investigation on the interaction between IGFBP3 and NF-κB in the context of AF is warranted to offer a molecular basis for the mechanisms in the pathogenesis of AF. The gene discussed is NFKB1; the disease is atrial fibrillation.