Moreover, a post-hoc analysis of a prospective, single-centre cohort study of 907 patients with non-valvular atrial fibrillation (AF), demonstrated, in vivo, that circulating levels of PCSK9 and LPS are associated with a mechanism possibly involving NADPH oxidase activation, as both LPS and PCSK9 are correlated with Nox2 activation, and patients with concomitant increase in PCSK9 and LPS showed a higher risk of CVEs [48]. The gene discussed is PCSK9; the disease is atrial fibrillation.