In an observational study of 100 consecutive patients, including 80 patients with a first diagnosis of AF and 20 control patients, it was found that pro-inflammatory and cytotoxic T-lymphocyte subpopulations (CD8+) circulate more frequently during early AF compared with patients without AF and are accompanied by increased levels of plasma CD8+ effector molecules.[18] Activated CD8+ T cells perform by releasing cytotoxins (perforin, granzyme and granulysin) or by releasing the secretion of pro-inflammatory cytokines, such as TNF-α and IFN-γ to induce apoptosis in target cells.[39,40]. Here, CD8A is linked to atrial fibrillation.