There is also some evidence that plaque development and rupture is influenced directly by viral infection of vascular cells.45 Similarly, peripheral immune responses to viral infections are thought to contribute to the pathogenesis of AF through the release of reactive oxygen species and myeloperoxidases from neutrophils and the local release of TNF-α and IL-1β from macrophages.46 Viral infection may also be an important factor in the development of non-valvular AF through upregulation of monocyte TLR2 and IL-6 release.47 The gene discussed is TLR2; the disease is viral infectious disease.