Although clinical relevance of increased NAP-2 concentrations in AF patients remains to be established, the current data suggests that NAP-2 could be a novel factor involved in the AF pathogenesis and associated thromboembolism, which highlight the complexity of interactions among enhanced oxidative stress, inflammation and prothrombotic state in AF and the need for novel therapeutic approaches beyond anticoagulation to prevent stroke or systemic thromboembolism. This evidence concerns the gene PPBP and atrial fibrillation.