Given the aforementioned propensity for blood stasis in the presence of diminished atrial wall motility and associated risk for thromboembolism, the present study sought to investigate potential intersections of LASp and platelet reactivity, as well as the involvement of the inflammatory mediators C-reactive protein (CRP) and Txnip, in a cohort of AF patients. The gene discussed is CRP; the disease is atrial fibrillation.